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MCM7 (minichromosome maintenance complex component 7)

Written2020-09Keli Lima, Eduardo Magalhães Rego, João Agostinho Machado-Neto
Laboratory of Medical Investigation in Pathogenesis and Targeted Therapy in Onco-Immuno-Hematology (LIM-31), Department of Hematology, Hospital das Clènicas HCFMUSP, Faculdade de Medicina, University of São Paulo, São Paulo, Brazil (KL, EMR); Department of Pharmacology, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil (KL, JAM-N); (KL); (EMR); (JAM-N)

Abstract MCM7 belongs to the minichromosome maintenance (MCM) protein family, which compromises DNA helicases that play a key role in DNA replication and G1/S cell cycle progression. There are plenty of studies on MCM7 expression for cancer development and progression. Increased levels of MCM7 are consistently implicated in high aggressiveness characteristics and poor clinical outcomes in several cancer types. In the present review, the data on DNA/RNA, the protein encoded, and the implication of MCM7 as diagnostic, prognostic, and biological values in cancer are described.

Keywords MCM7; Cell cycle; DNA replication; G1/S Transition; Adrenocortical carcinoma; Adrenocorticotropin secreting tumors; Bladder cancer; Breast cancer; Cervical cancer; Colorectal cancer; Cutaneous diseases; Desmoid cancer; Endometrial cancer; Head and neck cancer; Hepatocellular carcinoma; Gastric cancer; Gliomas; Leukemia; Lymphoma; Lung cancer; Medulloblastoma; Meningiomas; Neuroblastoma; Pancreatic cancer; Pituitary adenoma; Prostate cancer; Renal cancer; Retinoblastoma; Squamous cell carcinoma; Synovial sarcoma; Thyroid cancer

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Alias (NCBI)MCM2
HGNC (Hugo) MCM7
HGNC Alias symbCDC47
HGNC Alias nameprotein phosphatase 1, regulatory subunit 104
HGNC Previous nameMCM2
HGNC Previous nameminichromosome maintenance deficient (S. cerevisiae) 7
 MCM7 minichromosome maintenance deficient 7 (S. cerevisiae)
LocusID (NCBI) 4176
Atlas_Id 41323
Location 7q22.1  [Link to chromosome band 7q22]
Location_base_pair Starts at 100092728 and ends at 100100780 bp from pter ( according to GRCh38/hg38-Dec_2013)  [Mapping MCM7.png]
Fusion genes
(updated 2017)
Data from Atlas, Mitelman, Cosmic Fusion, Fusion Cancer, TCGA fusion databases with official HUGO symbols (see references in chromosomal bands)


Description The entire MCM7 gene is approximately 9.2 Kb (start: 100092728 and end: 100101940 bp; orientation: reverse strand). In the NCBI database (, there are 3 transcript variants for CDC7 that encode for the 2 protein isoforms. The transcript variant 1 (transcript length: 2467 bp); encodes the longer protein, isoform 1 (719 aa). The transcript variant 2 (transcript length: 2996 bp) and 3 (transcript length: 2542 bp) encodes the short protein, isoform 2 (543 aa). Both transcript variants, 2 and 3, contain an additional internal segment that leads to translation initiation from an in-frame downstream AUG compared to transcript variant 1, which leads to a shorter N-terminus. In Ensembl database (, there are ten additional transcript variants for MCM7, two are protein coding transcripts (ENST00000343023.10: 1968 bp and 389 aa, and ENST00000425308.5: 1497 bp and 183 aa), one is a nonsense-mediated mRNA decay (ENST00000491245.6: 648 bp and 83 aa) and seven are non-protein-coding transcripts.


  Figure 1. Schematic MCM7 protein structure. (A) MCM7 protein presents two isoforms (isoform 1: 719 aa, isoform 2: 543 aa) and contains a minichromosome maintenance (MCM) domain. The position of amino acids (aa) is indicated in the Figure. The 3D reconstitution of the isoform 1 of MCM7 protein was constructed using the Swiss-model platform (, and cartoon (B) and surface (C) versions of the protein are illustrated.
Description Two MCM7 isoforms are better described: the isoform 1 consists of 719 amino acids (aa), while isoform 2 consists of 543 aa, both isoforms present a conserved MCM domain in the C-terminal region. The schematic representation of the MCM7 isoforms are illustrated in Figure 1.
Expression Ubiquitous.
Localisation Cytoplasm and nucleus. The nuclear import of MCM proteins occurs as a complex.
Function MCM7 belongs to the minichromosome maintenance (MCM) protein family, which compromises DNA helicases important for initiating DNA replication and for cell cycle progression (Forsburg, 2008; Lo Sardo et al., 2017). This protein family consists of at least six members (MCM2-7) that have been implicated in the regulatory machinery to ensure DNA synthesis happens once per cell cycle. During the G1 phase of the cell cycle, the MCM complex is inactive around the double DNA strand at the replication origins. In the S phase of the cell cycle, there is the recruitment of helicase cofactors, CDC45 and GINS, for the MCM complex (forming the CMG complex) that activates its activity, translocating it in the 3' to 5' direction along the DNA enabling the replisome assembly. The head-to-head configuration of the MCM complexes provides bidirectional DNA synthesis (Hyrien, 2016). Although uncomplexed MCM7 did not present ATPase or DNA helicase activity, it plays an essential for DNA helicase activity of the MCM complex (Figure 2). MCM7 expression is regulated by E2F transcription factors under growth factor stimulation by PI3K/AKT/ GSK3B / CCND1 / RB1 axis (Ishimi, 2018; Suzuki et al., 1998; Yoshida and Inoue, 2004). MCM7 is a marker of cell proliferation and its aberrant expression contributes to tumor development and progression (Honeycutt et al., 2006).
  Figure 2. Model for MCM7 function in DNA replication. MCM7 is a component of minichromosome maintenance (MCM) complex (MCM2-7), forming a hexameric ring that binds to DNA and acts as a replication licensing. The recruitment of CDC45 and GINS is required for helicase activity of the complex (CMG complex). Upon DNA unwinding, occurs the formation of replication forks in the double stranded DNA at origin and DNA synthesis by the recruitment of DNA polymerases.
Homology MCM7 has high homology among different species (Table 1).
Table 1. Comparative identity of human MCM7 with other species
% Identity for: Homo sapiens BIRC7SymbolProteinDNA
vs. P. troglodytesMCM7 99.9 99.4
vs. M. mulattaMCM7 98.4 96.4
vs. C. lupus MCM7 96.2 88.7
vs. B. taurus MCM7 96.4 89.3
vs. M. musculus Mcm7 92.8 86.9
vs. R. norvegicus Mcm7 94.3 87.1
vs. X. tropicalis mcm7 84.8 74.1
vs. D. rerio mcm7 80.8 73.6
vs. D. melanogaster Mcm7 67.5 63.7
vs. A. gambiae AgaP_AGAP005800 67.0 64.2
vs. C. elegans mcm-7 52.5 54.6
vs. S. cerevisiae MCM7 50.1 51.2
vs. K. lactis KLLA0E23189g 52.2 52.1
vs. E. gossypii AGOS_ADR041W 50.7 54.0
vs. S. pombe mcm7 50.8 51.7
vs. M. oryzae MGG_09300 50.8 54.6
vs. N. crassa NCU08119 52.4 56.4
vs. A. thaliana PRL 52.4 53.7
vs. O. sativa Os12g0560700 50.9 53.1



Somatic Recurrent mutations in the MCM7 gene are rare. A total of 596 out of 47005 (1.3%) tested samples presented MCM7 genetic alterations (mutations, amplifications, deep deletions, and multiple alterations), as reported on cBioPortal ( A total of 218 somatic mutations (0.5% of the samples) was found: 170 missense substitutions, 42 truncating, 4 inframe, and 2 other mutations. In COSMIC (Catalogue of Somatic Mutations in Cancer; data base, a total of 465 (1.2%) unique samples presenting MCM7 mutations were found among the 37667 samples tested, being 200 missense substitutions, 81 synonymous substitutions, 28 nonsense substitutions, 11 frameshift deletions, 3 frameshift insertions, 2 inframe deletions and 1 inframe insertion, and 60 other mutations.

Implicated in

Entity Adrenocortical carcinomas
Note MCM7 was identified as a potential diagnosis marker for distinguishing benign tumors from malignant adrenocortical tumors (Aporowicz et al., 2019).
Garbicz and colleagues (Garbicz et al., 2017) reported a significant increase of MCM7 expression in ACTHomas. In addition, MCM7 was ubiquitously overexpressed in Crooke cell adenomas and a combination of MCM7 and MIR106B - MIR25 expressions accurately differentiated invasive from non-invasive tumors and predicted postoperative tumor recurrence/progression.
Entity Bladder cancer
Note Atypical inverted papilloma presented increased MCM7 levels compared to typical papilloma, which was associated with higher proliferative activity induced by HPV infection. In addition, MCM7 expression was observed predominantly in the nucleus and, to a lesser extent, weakly in the cytoplasm (Shigehara et al., 2011a). In another study, the authors reported that the MCM7 expression in normal bladder mucous or HPV-negative bladder tissues was lower compared to HPV-positive tumors (Shigehara et al., 2011b). In a papillomavirus-associated bladder carcinoma case study, it was shown that MCM7 was highly expressed both in the basal cells of the condyloma tissue and in the basal layer of the tumor tissues (Kawaguchi et al., 2012). In a multicenter bladder cancer cohort (576 patients), MCM7 expression was an independent prognostic factor for disease progression (Fristrup et al., 2013).
Higher MCM7 expression was found in T24R2, a cisplatin-resistant bladder cancer cell line compared to T24, a cisplatin-sensitive bladder cancer cell line, suggesting a potential role for MCM7 in chemoresistance (Kim et al., 2016).
Entity Breast cancer
Note The expression of MCM7 was significantly higher in tumor than in adjacent non-tumor tissues, suggesting a potential role for this protein in the tumor development and progression (Lu et al., 2011; Song et al., 2006). In MCF-7 breast cancer cells, MCM7 participates in the MYB network and it was up-regulated by exposure to estradiol (Wu et al., 2012). Treatment with cantharidin inhibits the expression of MCM7, reducing cell proliferation, in MCF-7 cells (Zhang and Yan, 2015). In addition, the downregulation of MCM7 upregulated γH2AX (phosphorylated H2AX) in tamoxifen-resistant MCF7 and T47D breast cells (Liang et al., 2017).
Entity Cervical cancer
Note MCM7 interacts with E6 viral protein from HPV, which may be implicated in chromosomal abnormalities and cell transformation (Kukimoto et al., 1998). In cervical lesions associated with HPV-16, MCM7 expression was higher in intraepithelial lesions, and the highest levels were observed in cancer (Brake et al., 2003). Similarly, the expression of MCM7 presented a predictive value of cervical cancer severity with 94.0% sensitivity, 56.5% specificity, 88.8% positive predictive value, and 72.2% negative predictive value (Zhang et al., 2013).
Entity Colorectal cancer
Note MCM7 expression was an independent prognostic factor for colorectal cancer, and MCM7-positive tumors correlated with increased metastasis rates (Nishihara et al., 2008). High MCM7 expression was also associated with adverse clinical outcome in colorectal cancer patients who underwent surgery for the primary tumor (Pillaire et al., 2010). In agreement, MCM7-positive Dukes' C colorectal cancer patients presented lower overall survival and event-free survival (Ishibashi et al., 2014). Using quantitative PCR, Shi and colleagues (Shi et al., 2018) reported that MCM7 is one of the main genes involved in colorectal cancer progression. Recently, a meta-analysis has indicated MCM7 as a potential biomarker for colorectal cancer (Long et al., 2016).
Using a cohort of 13 anal cancer patients treated with radiation or without additional chemotherapy, Bruland and colleagues (Kreuter et al., 2010) described that the MCM7 protein was associated with better relapse-free survival and cancer-specific survival. The authors also highlighted that MCM7 may be regulated by the transcription factor E2F and induced by HPV. In anal intraepithelial high-grade neoplasm, the MCM protein family, including MCM7, was a marker of high-grade lesions and HPV-DNA load (Kreuter et al., 2010).
Entity Cutaneous diseases
Note Using malignant and premalignant cultured cells from cutaneous diseases, Hiraiwa and colleagues (Hiraiwa et al., 1998) reported that MCM7 expression presented good correlations with clinical, microscopic, and biological malignancy characteristics.
Entity Desmoid cancer
Note Using microarray analysis, low MCM7 was observed in desmoid tumors, which may be associated with the reduced mitotic activity observed in this kind of tumors (Ferenc et al., 2010).
Entity Endometrial cancer
Note High MCM7 was a reliable marker for the diagnosis of endometrial carcinoma, which was also associated with high histological grade and poor survival outcomes (multivariate analysis) (Li et al., 2005). Similarly, MCM7 expression was upregulated in endometrial cancer compared to the normal adjacent tissues (Zhao et al., 2012).
Entity Head and neck cancer
Note Microarray analysis identified MCM7, among the six genes overexpressed in hypopharyngeal tumors, which was also associated with disease aggressiveness (Cromer et al., 2004). Similarly, MCM7 was increased in salivary tumors compared to normal salivary tissues and the high MCM7 expression was associated with advanced stage, invasion of adjacent tissue, invasion of the nerve, and poor clinical outcomes (Wen et al., 2018).
Using a murine model of head and neck squamous cell carcinoma, MCM7 was found as a potential biomarker for distinguishing HPV-positive and HPV-negative tumors (Strati et al., 2006).
Entity Hepatocellular carcinoma
Note MCM7 expression was higher in hepatocellular carcinoma compared with non-tumor liver samples (Iizuka et al., 2006; Karavias et al., 2016; Qu et al., 2017; Wang et al., 2019; Yen et al., 2016). MCM7-positive hepatocellular carcinoma was associated with hepatitis, intrahepatic metastasis, vascular invasion, cell differentiation, tumor size, and shorter overall survival (Qu et al., 2017; Wang et al., 2019; Zhou et al., 2012).
In a cohort of 1300 cases of HBV-positive hepatocellular carcinoma, 1344 HBV-persistent, and 1344 individuals with natural HBV clearance, the AG/GG genotypes of the MCM7 polymorphism, rs999885, presented a decreased risk of chronic HBV infection in natural HBV clearance subjects. On the other hand, AG/GG genotypes negatively impacted the risk for the development of hepatocellular carcinoma in HBV persistent carriers (Liu et al., 2012a).
In univariate analysis, the G/G genotype of polymorphism in MCM7, rs2070215, impacted the risk for the development of the disease in a cohort containing 1019 hepatocellular carcinoma patients and 1138 healthy individuals (Nan et al., 2016). In hepatoma cells, MCM7 was downregulated by histone deacetylase inhibitor SAHA (Yang et al., 2015).
MCM7 shRNA lentivirus-mediated silencing reduced malignant behavior, suppressing proliferation, cell cycle progression, survival, and invasiveness, in MHCC-97H cells (Liu et al., 2015). Similarly, MCM7 silencing significantly reduced cellular proliferation in vitro and hepatocellular carcinoma tumorigenicity in vivo (Qu et al., 2017).
Using bioinformatics tools, MCM7 gene expression was identified as a potential biomarker for diagnosis and prognosis in hepatocellular carcinoma (Liao et al., 2018b; Liu et al., 2019). MCM7 expression was found to be a complementary and more effective prognostic marker compared to alpha-fetal protein in hepatocellular carcinoma (Xiang et al., 2019; Yu et al., 2018). Therefore, MCM7 was also identified as a protein with clinical relevance in hepatocellular carcinoma by PCT-SWATH (pressure-cycling technology applied to sequential window acquisition of all theoretical mass spectra) (Zhu et al., 2019).
Arsenic trioxide reduced MCM7 expression, which recapitulates the effects of MCM7 silencing on tumor suppression murine models of hepatocellular carcinoma, suggesting that arsenic trioxide may benefit from the treatment of this disease (Wang et al., 2019).
Entity Gastric cancer
Note Using array comparative genomic hybridization, the amplification of 7q22.1 was observed in samples from gastroesophageal adenocarcinomas, and despite the positive correlation between the expression of MCM7 mRNA and protein, no association was observed with the genomic data (van Dekken et al., 2009).
MCM7 expression was upregulated in tumors compared to non-tumor gastric tissues, and its nuclear expression was associated with advanced age and poor disease-specific survival. In normal gastric epithelial tissue, MCM7 was strictly expressed in the proliferative compartment (Kang et al., 2014). Of note, the combination of MCM7 and Ki-67 was a more sensitive proliferation marker to identify esophageal cancer, gastric carcinoma, and precancerous lesions (Huber et al., 2015; Yang et al., 2018).
MCM7 knockdown, by siRNA, suppressed cell proliferation, colony formation, and invasion, and induced late apoptosis in gastric cancer cell lines (Kang et al., 2014).
Entity Gliomas
Note Bioinformatics tools identified that the genomic region containing the MCM7 gene was amplified in more than 80% of the present cases and quantitative PCR confirmed the upregulation of MCM7 in glioblastomas compared to normal tissues (Erkan et al., 2014). In grade II-IV gliomas, increasing MCM7 expression was an independent predictor of poor overall survival (Hua et al., 2014). Using immunohistochemistry, MCM7 was found to a better marker for identifying cells into cell cycle progression than MKI67 (Ki-67) and PCNA in glioblastoma (Facoetti et al., 2006).
In glioblastoma models, siRNA-mediated MCM7 knockdown reduced cell proliferation and inhibited tumor growth in the xenograft and orthotopic glioblastoma models in rats (Erkan et al., 2014).
Entity Leukemia
Note The single nucleotide polymorphisms in MCM7, rs2070215, rs1534309, rs2307355, and rs17447273, were not associated with AML risk (103 AML patients and 241 healthy individuals), but the rs2070215 significantly associated with AML relapse and the C/C genotype of rs1534309 positively impacted on the survival of AML patients (Lee et al., 2017). The impact of single nucleotide polymorphisms on MCM7, rs2070215, rs1527423, and rs1534309, was also investigated in a cohort of 281 acute myeloid leukemia patients and 405 healthy individuals, and the allele C of rs2070215 presented an increased frequency in AML patients (Tripon et al., 2020). In addition, among the eight different haplotypes, two (G/A/T and C/A/T for rs1534309/rs1527423/rs2070215, respectively) were associated with AML risk, regardless of age and gender (Tripon et al., 2020).
Higher MCM7 expression was observed at relapse when compared to the time of diagnosis in MLL-rearranged pediatric acute myeloid leukemia (Verboon et al., 2016). In chronic myeloid leukemia cells, K562, MCM7 is highly expressed and its silencing by siRNA exerts anti-proliferative and pro-apoptotic effects (Tian et al., 2017)
Entity Lymphoma
Note In Hodgkin's lymphoma, MCM7 is highly expressed in asymptomatic patients. High MCM7 expression was associated with greater age, advanced stage of the disease, and negatively impacted overall survival in multivariate analysis (Marnerides et al., 2011). Using immunohistochemistry, MCM7 was found to be more frequently positive in primary cutaneous T-cell lymphoma samples compared to benign inflammatory dermatosis, and it was also correlated with Ki-67 and MCM3 expression (Jankowska-Konsur et al., 2015).
In lymphoproliferative skin disorders of T cells, MCM7 levels were observed in a greater expression of mycosis fungoides IIB--V and lymphomatoid papulosis compared to parapsoriasis in plaque and mycosis fungoides stage I-IIA (Gambichler et al., 2008).
Entity Lung cancer
Note Fujioka and colleagues (Fujioka et al., 2009), evaluating MCM7 and Ki-67 expressions in lung adenocarcinoma, found that MCM7 may be an independent prognostic marker, especially in early-stage tumors. MCM7-positive cells were absent in non-neoplastic alveolar epithelia and it was significantly higher in the peripheral area of the tumor (Fujioka et al., 2009). High scores for MCM7 expression were correlated with male gender, high histological grade, worse histological subtype, and increased tumor size and worse prognosis. Latterly, the same research group has shown how MCM7 expression was decisive for the creation of a prognostic score, based on proteins expressed in different phases of the cell cycle. Thus, the scores containing proteins expressed in G1/S (MCM7+/Ki-67+/Geminin+) and S/G2/M (MCM7+/ AURKA +/p-Histone H3S10+) presented worse clinical outcomes than MCM7-negative patients (G0) (Haruki et al., 2012).
In agreement, another study reported that MCM7 expression was significantly higher in lung cancer tissues, and its high expression correlated with poor prognosis in non-small cell lung cancer (Toyokawa et al., 2011). The authors also showed that combination therapy of histone deacetylase inhibition by a novel HDAC inhibitor, YF454A, with erlotinib to overcome EGFR -TKI resistance in in vitro and in vivo non-small cell lung cancer growth, by blocking MCM7 expression (Toyokawa et al., 2011).
In squamous cell carcinoma and lung adenocarcinoma, MCM7 levels in bronchial brushings were correlated with patient gender, tumor type, and tumor location (Liu et al., 2012b), indicating that MCM7 may be used as a protein marker for the early detection of bronchial brushing lung cancer (Liu et al., 2014). Recently, the role of MCM7 as a diagnosis marker for lung cancer has been confirmed by employing the Granger causality test (Fan et al., 2019).
Zhong and colleagues (Zhong et al., 2014a; Zhong et al., 2014b) reported that positive MCM7 expression was associated with positive NEK2 and Ki-67 expression, which was an independent prognostic factor for survival in resected non-small cell lung cancer patients, and the combined expression of MCM7/Ki-67 with NEK2 improved prognostic prediction, in which patients who had positive NEK2 expressions and positive MCM7/Ki-67 presented a lower survival rate than patients with negative expressions for these markers (Zhong et al., 2014a; Zhong et al., 2014b).
In non-small cell lung cancer cells, MCM7 phosphorylation was regulated by RACK1 through the MCM7/RACK1/AKT complex, resulting in an increase of the oncogenic potential of these cells (Fei et al., 2017). MCM7 expression had also been correlated with LMNB2 levels, and the high expression of both proteins was correlated with high tumor TNM stage, moderate-poor differentiation, and shorter overall survival of non-small cell lung cancer patients (Ma et al., 2017). Lo Sardo and colleagues (Lo Sardo et al., 2017) added novel insights for MCM7-mediated oncogenic pathways in lung cancer, by the interaction of MCM7 and YAP1 / TAZ, which impacted cell proliferation by CDKN1A inhibition.
Entity Medulloblastoma
Note MCM7 overexpression increased anchorage-independent cell growth, migration, and invasion in medulloblastoma cells (Lau et al., 2010).
Entity Meningioma
Note MCM7 was highly expressed in meningioma compared to arachnoid tissues (Saydam et al., 2010), suggesting a potential role for this protein as a diagnostic marker. Similar findings were observed in recurrent meningiomas compared with non-recurrent meningiomas and the ROC curve indicated that MCM7 expression had a high sensitivity for disease recurrence (Winther and Torp, 2017). A higher percentage of MCM7-positive cells was also associated with reduced recurrence-free survival in multivariate analysis (Winther and Torp, 2017).
Entity Neuroblastoma
Note In neuroblastoma, MCM7 was found to be a target of MYCN transcription factor, once it is highly expressed in tumors with MYCN amplification (Shohet et al., 2002). In contrast, another study indicated that MCM7 overexpression is not necessarily correlated with MYCN amplification or an aggressive clinical course in neuroblastoma (Tsai et al., 2004).
Functional assays using a neuroblastoma cell line with inducible MYCN expression indicated that the increased rate of cells entering the S-phase and enhancing DNA replication machinery may be associated with the expression of MCM7 (Koppen et al., 2007).
Entity Ovarian cancer
Note In a cohort of 342 ovarian cancer patients, increased MCM7 expression was observed in high-grade serous tissues (Ota et al., 2011). Similar findings were reported by Kobierzycki and colleagues (Kobierzycki et al., 2013). In contrast, higher MCM7 expression was associated with better progression-free survival (Ota et al., 2011).
Entity Pancreatic cancer
Note Using microarray and immunohistochemistry analysis, high MCM7 expression was found in samples from pancreatic ductal adenocarcinoma patients (Grutzmann et al., 2004; Liang et al., 2014). In agreement, the MCM family, including MCM7, has been upregulated in pancreatic tumor tissues (Liao et al., 2018a).
In a retrospective cohort of pancreatic neuroendocrine neoplasm patients (n=156), the high expression of MCM7 was significantly associated with larger tumor size, non-functioning tumor, high grade, and TNM stage, and it was an independent prognostic factor for tumor progression (Ban et al., 2019).
Entity Pituitary adenoma
Note High nuclear MCM7 expression was associated with a shorter recurrence/progression-free survival in a cohort of 97 pituitary adenoma patients. Moreover, among patients with invasive tumors, high MCM7 identified those with the highest risk of recurrence/progression (Coli et al., 2016).
Entity Prostate cancer
Note Comparing MCM7 and Ki-67 expression as proliferation markers in prostate cancer, MCM7 was a better discriminatory marker for proliferation between benign epithelium, prostatic intraepithelial neoplasia, and invasive adenocarcinoma (Levesque et al., 2007; Majid et al., 2010; Padmanabhan et al., 2004).
MCM7 amplification or overexpression was associated with relapse, local invasion, and worse degree of the tumor (Ren et al., 2006). In prostate cancer patients treated with prostatectomy, high MCM7 was associated with a high Gleason score and was an independent shorter progression-free survival factor (Laitinen et al., 2008). Similar findings were reported by Tolonem and colleagues (Tolonen et al., 2011).
Evaluating cell proliferation and apoptosis profile in prostate aging in adult male Wistar rats, MCM7 was identified as a promising marker for the early detection of pre-malignant diseases (Gonzaga et al., 2017).
In DU145 cells, constitutive MCM7 expression resulted in marked DNA synthesis, cell proliferation, and invasion in vitro assays, and larger tumors and reduced mice survival in vivo assay (Ren et al., 2006). In agreement, MCM7 inhibition decreased tumor volume, metastases, and improved survival in xenograft DU145 and PC3 tumors mice (Shi et al., 2010).
Entity Renal cancer
Note The levels of expression of the members of the MCM family, including MCM7, were higher in renal cell carcinoma compared to the paired adjacent normal tissue. Primary renal cell carcinoma patients overexpressing two or more MCM-related genes and metastatic renal cell carcinoma patients overexpressing three or more MCM-related genes presented shorter disease-free survival (Zhong et al., 2017).
Entity Retinoblastoma
Note Using data-mining tools and validation by real-time RT-PCR and tissue microarrays in retinoblastoma and normal human retina samples, MCM7 was identified as a potential therapeutic target in retinoblastoma (Yang et al., 2008).
Entity Squamous cell carcinomas
Note Using a murine model with deregulated MCM7 expression on the basal layer of the epidermis, Honeycutt and colleagues (Honeycutt et al., 2006) concluded that MCM7 actively contributes to the formation of tumors, progression and malignant conversion of squamous cell carcinomas of the skin.
Increased MCM7 expression was associated with lymph node metastasis and high tumor grade in precancerous lesions and oral squamous cell carcinoma (Feng et al., 2008). In agreement, MCM7 expression was highly expressed in dysplasias and oral squamous cell carcinoma compared to normal epithelia, and its aberrant expression was associated with high histological grade, poorly differentiated tumors, and poor survival outcomes (Tamura et al., 2010).
In oesophageal squamous cell carcinoma, MCM7 was also associated with histological factors, tumor depth, lymph node metastasis, tumor stage, and G9a expression. Double-positive expression for EHMT2 (G9a) and MCM7 oesophageal squamous cell carcinoma patients (G9a+/MCM7+) presented shorter survival compared to those with low G9a or MCM7 expression (G9a-/MCM7-), (G9a+/MCM7-), (G9a-/MCM7+) (Zhong et al., 2015). Recently, Qiu and colleagues (Qiu et al., 2017) have reported that MCM7 is amplified in 12% of esophageal squamous cell carcinomas and > 4% of head and neck squamous cell carcinomas and stomach carcinomas patients from the TCGA data. MCM7 overexpression was confirmed in three GEO independent data sets for esophageal cancer. MCM7 silencing by siRNAs inhibited cell proliferation, colony formation, and migration in KYSE510 and EC9706 cells. MCM7 depletion also suppressed AKT/mTOR activation, and cell cycle-related regulatory proteins, CCND1, CCNE2, and CDK2 (Qiu et al., 2017).
MCM7 expression significantly correlated with Ki-67, BMI1, and CCNE1 expression, and MCM4 and MCM7 were sensitive proliferation markers in esophageal carcinoma and precancerous lesions (Choy et al., 2016). Using bioinformatics analysis of gene expression data, Wang and colleagues (Wang et al., 2015) highlighted that MCM7 belongs to critical genes for head and neck squamous cell carcinoma.
In laryngeal squamous cell carcinoma, MCM7 expression was associated with EGFR (HER1) expression, and its high expression increased risk for disease progression, benign an independent prognostic factor overall survival, and progression-free survival (Almadori et al., 2017). In addition, MCM7 expression presented a strong correlation with Ki-67 in laryngeal squamous cell cancer (Nowinska et al., 2016).
Entity Synovial sarcoma
Note MCM7 was found to be a target of MYCN in synovial sarcoma (Somers et al., 2007).
Entity Thyroid cancer
Note Using cDNA array, MCM7 upregulation was observed in malignant thyroid neoplasms compared to benign thyroid neoplasms, being more expressed in high graded and locally invasive tumors. MCM7 combined with MCM5 and RAD9A mRNA levels showed 98.2% sensitivity and 65.7% specificity as a predictor of malignancy (Kebebew et al., 2006). In anaplastic thyroid carcinoma cells, MCM7 was overexpressed compared to normal thyroid cells, which was related to TP53 activity (Guida et al., 2005).

To be noted

The prognostic value and biological function of MCM7 for oncogenesis have been extensively studied in several types of cancer. In general, increased levels of MCM7 are implicated in poor clinical outcomes. In addition, functional studies have indicated that high MCM7 expression promoted cell cycle progression, proliferation, migration, and invasion in in vitro and in vivo studies.
Acknowledgments: This study was supported by the grant #2019/23864-70, São Paulo Research Foundation (FAPESP), and grant #402587/2016-2, Conselho Nacional de Desenvolvimento Cientèfico e Tecnológico (CNPq). The authors thank Fernanda T. Udinal, from the Hemocentro Foundation of Ribeirão Preto, São Paulo, Brazil, for the English language review.


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Zhu Y, Zhu J, Lu C, Zhang Q, Xie W, Sun P, Dong X, Yue L, Sun Y, Yi X, Zhu T, Ruan G, Aebersold R, Huang S, Guo T
Proteomics Clin Appl 2019 Jan;13(1):e1700179.
PMID 30365225
Array comparative genomic hybridization, expression array, and protein analysis of critical regions on chromosome arms 1q, 7q, and 8p in adenocarcinomas of the gastroesophageal junction
van Dekken H, Tilanus HW, Hop WC, Dinjens WN, Wink JC, Vissers KJ, van Marion R
Cancer Genet Cytogenet 2009 Feb;189(1):37-42.
PMID 19167610


This paper should be referenced as such :
Lima K, Rego EM, Machado-Neto JA
MCM7 (minichromosome maintenance complex component 7);
Atlas Genet Cytogenet Oncol Haematol. in press

External links


HGNC (Hugo)MCM7   6950
Atlas Explorer : (Salamanque)MCM7
Entrez_Gene (NCBI)MCM7    minichromosome maintenance complex component 7
AliasesCDC47; MCM2; P1.1-MCM3; P1CDC47; 
P85MCM; PNAS146; PPP1R104
GeneCards (Weizmann)MCM7
Ensembl hg19 (Hinxton)ENSG00000166508 [Gene_View]
Ensembl hg38 (Hinxton)ENSG00000166508 [Gene_View]  ENSG00000166508 [Sequence]  chr7:100092728-100100780 [Contig_View]  MCM7 [Vega]
ICGC DataPortalENSG00000166508
TCGA cBioPortalMCM7
AceView (NCBI)MCM7
Genatlas (Paris)MCM7
SOURCE (Princeton)MCM7
Genetics Home Reference (NIH)MCM7
Genomic and cartography
GoldenPath hg38 (UCSC)MCM7  -     chr7:100092728-100100780 -  7q22.1   [Description]    (hg38-Dec_2013)
GoldenPath hg19 (UCSC)MCM7  -     7q22.1   [Description]    (hg19-Feb_2009)
GoldenPathMCM7 - 7q22.1 [CytoView hg19]  MCM7 - 7q22.1 [CytoView hg38]
Genome Data Viewer NCBIMCM7 [Mapview hg19]  
Gene and transcription
Genbank (Entrez)AF279900 AI083651 AK055379 AK096959 AK226175
RefSeq transcript (Entrez)NM_001278595 NM_005916 NM_182776
Consensus coding sequences : CCDS (NCBI)MCM7
Gene ExpressionMCM7 [ NCBI-GEO ]   MCM7 [ EBI - ARRAY_EXPRESS ]   MCM7 [ SEEK ]   MCM7 [ MEM ]
Gene Expression Viewer (FireBrowse)MCM7 [ Firebrowse - Broad ]
GenevisibleExpression of MCM7 in : [tissues]  [cell-lines]  [cancer]  [perturbations]  
BioGPS (Tissue expression)4176
GTEX Portal (Tissue expression)MCM7
Human Protein AtlasENSG00000166508-MCM7 [pathology]   [cell]   [tissue]
Protein : pattern, domain, 3D structure
UniProt/SwissProtP33993   [function]  [subcellular_location]  [family_and_domains]  [pathology_and_biotech]  [ptm_processing]  [expression]  [interaction]
NextProtP33993  [Sequence]  [Exons]  [Medical]  [Publications]
With graphics : InterProP33993
Catalytic activity : Enzyme3.6.4.12 [ Enzyme-Expasy ] [ IntEnz-EBI ] [ BRENDA ] [ KEGG ]   [ MEROPS ]
Domaine pattern : Prosite (Expaxy)MCM_1 (PS00847)    MCM_2 (PS50051)   
Domains : Interpro (EBI)AAA+_ATPase    MCM    MCM7    MCM_CS    MCM_dom    MCM_lid    MCM_N    MCM_OB    NA-bd_OB-fold    P-loop_NTPase   
Domain families : Pfam (Sanger)MCM (PF00493)    MCM_lid (PF17855)    MCM_N (PF14551)    MCM_OB (PF17207)   
Domain families : Pfam (NCBI)pfam00493    pfam17855    pfam14551    pfam17207   
Domain families : Smart (EMBL)AAA (SM00382)  MCM (SM00350)  
Conserved Domain (NCBI)MCM7
PDB Europe6XTX    6XTY   
PDB (PDBSum)6XTX    6XTY   
PDB (IMB)6XTX    6XTY   
Structural Biology KnowledgeBase6XTX    6XTY   
SCOP (Structural Classification of Proteins)6XTX    6XTY   
CATH (Classification of proteins structures)6XTX    6XTY   
AlphaFold pdb e-kbP33993   
Human Protein Atlas [tissue]ENSG00000166508-MCM7 [tissue]
Protein Interaction databases
IntAct (EBI)P33993
Complex Portal (EBI)P33993 CPX-2940 MCM complex
Ontologies - Pathways
Ontology : AmiGOdouble-strand break repair via break-induced replication  chromosome, telomeric region  chromatin  DNA binding  DNA helicase activity  single-stranded DNA binding  protein binding  ATP binding  nucleus  nucleus  nucleoplasm  nucleoplasm  nucleolus  cytosol  DNA replication  DNA unwinding involved in DNA replication  DNA unwinding involved in DNA replication  DNA replication initiation  DNA strand elongation involved in DNA replication  cellular response to DNA damage stimulus  cell cycle  cell population proliferation  membrane  ATP hydrolysis activity  single-stranded DNA helicase activity  regulation of phosphorylation  MCM complex  MCM complex  MCM complex  MCM complex  CMG complex  CMG complex  cellular response to epidermal growth factor stimulus  cellular response to xenobiotic stimulus  
Ontology : EGO-EBIdouble-strand break repair via break-induced replication  chromosome, telomeric region  chromatin  DNA binding  DNA helicase activity  single-stranded DNA binding  protein binding  ATP binding  nucleus  nucleus  nucleoplasm  nucleoplasm  nucleolus  cytosol  DNA replication  DNA unwinding involved in DNA replication  DNA unwinding involved in DNA replication  DNA replication initiation  DNA strand elongation involved in DNA replication  cellular response to DNA damage stimulus  cell cycle  cell population proliferation  membrane  ATP hydrolysis activity  single-stranded DNA helicase activity  regulation of phosphorylation  MCM complex  MCM complex  MCM complex  MCM complex  CMG complex  CMG complex  cellular response to epidermal growth factor stimulus  cellular response to xenobiotic stimulus  
REACTOMEP33993 [protein]
REACTOME PathwaysR-HSA-69052 [pathway]   
NDEx NetworkMCM7
Atlas of Cancer Signalling NetworkMCM7
Wikipedia pathwaysMCM7
Orthology - Evolution
GeneTree (enSembl)ENSG00000166508
Phylogenetic Trees/Animal Genes : TreeFamMCM7
Homologs : HomoloGeneMCM7
Homology/Alignments : Family Browser (UCSC)MCM7
Gene fusions - Rearrangements
Fusion : MitelmanZNF3::MCM7 [7q22.1/7q22.1]  
Fusion : FusionHubC1ORF63--MCM7    GPC2--MCM7    IGJ--MCM7    KRT4--MCM7    MCM7--AGAP3    MCM7--BAIAP2L1    MCM7--C19ORF52    MCM7--C9ORF3    MCM7--CCT3    MCM7--FCF1   
MCM7--HACD3    MCM7--MBP    MCM7--MCM7    MCM7--MDC1    MCM7--TMTC3    POMGNT1--MCM7    PTGDS--MCM7    SBDSP1--MCM7    SCARA3--MCM7    SEMA4B--MCM7   
SETD5--MCM7    SNX29--MCM7    ZNF3--MCM7   
Fusion : QuiverMCM7
Polymorphisms : SNP and Copy number variants
NCBI Variation ViewerMCM7 [hg38]
dbSNP Single Nucleotide Polymorphism (NCBI)MCM7
Exome Variant ServerMCM7
GNOMAD BrowserENSG00000166508
Varsome BrowserMCM7
ACMGMCM7 variants
Genomic Variants (DGV)MCM7 [DGVbeta]
DECIPHERMCM7 [patients]   [syndromes]   [variants]   [genes]  
CONAN: Copy Number AnalysisMCM7 
ICGC Data PortalMCM7 
TCGA Data PortalMCM7 
Broad Tumor PortalMCM7
OASIS PortalMCM7 [ Somatic mutations - Copy number]
Somatic Mutations in Cancer : COSMICMCM7  [overview]  [genome browser]  [tissue]  [distribution]  
Somatic Mutations in Cancer : COSMIC3DMCM7
Mutations and Diseases : HGMDMCM7
LOVD (Leiden Open Variation Database)[gene] [transcripts] [variants]
DgiDB (Drug Gene Interaction Database)MCM7
DoCM (Curated mutations)MCM7
CIViC (Clinical Interpretations of Variants in Cancer)MCM7
NCG (London)MCM7
Impact of mutations[PolyPhen2] [Provean] [Buck Institute : MutDB] [Mutation Assessor] [Mutanalyser]
Genetic Testing Registry MCM7
NextProtP33993 [Medical]
Target ValidationMCM7
Huge Navigator MCM7 [HugePedia]
Clinical trials, drugs, therapy
Protein Interactions : CTDMCM7
Pharm GKB GenePA30697
Clinical trialMCM7
DataMed IndexMCM7
PubMed311 Pubmed reference(s) in Entrez
GeneRIFsGene References Into Functions (Entrez)
REVIEW articlesautomatic search in PubMed
Last year publicationsautomatic search in PubMed

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