Written | 2013-05 | Cansaran Saygili, Ayse Elif Erson-Bensan |
Department of Biological Sciences, Middle East Technical University, Ankara, Turkey |
Identity |
Alias (NCBI) | MIRN106B |
HGNC (Hugo) | MIR106B |
HGNC Alias symb | hsa-mir-106b |
HGNC Previous name | MIRN106B |
LocusID (NCBI) | 406900 |
Atlas_Id | 51084 |
Location | 7q22.1 [Link to chromosome band 7q22] |
Location_base_pair | Starts at 100093993 and ends at 100094074 bp from pter ( according to GRCh38/hg38-Dec_2013) [Mapping MIR106B.png] |
Local_order | miR-106b resides in the 13th intron of MCM7 (minichromosome maintenance complex component 7) gene. Genes flanking MCM7 are: - ZNF3 (7q22.1): zinc finger protein 3 - COPS6 (7q22.1): COP9 signalosome subunit 6 - MCM7 (7q21.3-7q22.1): minichromosome maintenance complex component 7 -- MIR106B (7q22.1): microRNA 106b -- MIR93 (7q22.1): microRNA 93 -- MIR25 (7q22.1): microRNA 25 - AP4M1 (7q22.1): adaptor-related protein complex4, mu 1 subunit - TAF6 (7q22.1): TAF6 RNA polymerase II, TATA box binding protein (TBP)-associated factor. |
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Figure 1. Genes flanking MCM7 gene on 7q22.1. → stands for positive strand, ← stands for negative strand. | |
Fusion genes (updated 2017) | Data from Atlas, Mitelman, Cosmic Fusion, Fusion Cancer, TCGA fusion databases with official HUGO symbols (see references in chromosomal bands) |
DNA/RNA |
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Figure 2. A. Genomic localization of miR-106b-25 members on chromosomal band 7q22.1. B. Stem loop structure of miR-106b. | |
Description | miR-106b is a member of microRNA cluster, miR-106b-25. All members of the cluster (miR-25, miR-93, miR-106b) reside in the 13th intron of MCM7 gene. |
Transcription | Pre-miRNA Length: 82 bp. Sequence: 5' CCUGCCGGGGCUAAAGUGCUGACAGUGCAGAUAGUGGUCCUCUCCGUGCUACCGCACUGUGGGUACUUGCUGCUCCAGCAGG 3' Mature miRNA Length: 21 bp Sequence: 12- 5' UAAAGUGCUGACAGUGCAGAU 3'- 32 (between 12th and 32nd nucleotides of the precursor miRNA). |
Pseudogene | No pseudogene was reported. |
Protein |
Note | miRNAs are not translated into aminoacids. |
Mutations |
Note | No mutations have been reported so far. However, a single nucleotide polymorphism (SNP), rs999885, was reported in the promoter region of miR-106b host gene (MCM7). A to G base change of rs999885 was suggested to have a protective role for chronic Hepatitis B virus (HBV) infection in AG/GG genotypes; however the same polymorphism was also linked to higher risk of hepatocellular carcinoma (HCC) in HBV carriers (Liu et al., 2012). Furthermore, expression level of miR-106b-25 cluster was found to be significantly higher in AG/GG individuals than in AA carriers in non-tumor liver tissues (Liu et al., 2012). |
Implicated in |
Note | |
Entity | Various cancers |
Note | Deregulated expression of miR-106b has been implicated in various tumor types. In connection, miR-106b is thought to play an important role in cell cycle progression by targeting CDKN1A (p21) and E2F1 which in turns increase the proliferation rate of cells. |
Entity | Gastric cancer |
Note | In a microarray study of 20 gastric primary tumors, miR-106b was shown to be upregulated together with miR-25 and miR-93 (other members of miR-106b-25 cluster) (Petrocca et al., 2008). Moreover, in a study conducted with 60 gastric cancer patients and 60 matched controls, plasma expression level of 15 selected microRNAs were measured by quantitative RT-PCR and 3 plasma microRNAs miR-106b, miR-20a, and miR-221 were found to be significantly increased. Hence, these microRNAs were suggested as potential bio-markers for early detection of gastric cancer (Cai et al., 2013). |
Entity | Esophageal adenocarcinoma |
Note | 5 esophageal cultured cells, 68 esophageal tissues (24 Barrett's esophagus, 22 esophageal adenocarcinoma and 22 normal epithelia) were analyzed by microarray to have a profile of differentially expressed miRNAs and miR-106b-25 cluster was shown to be upregulated in esophageal carcinoma (Kan et al., 2009). |
Entity | Prostate cancer |
Note | In a microarray study conducted with 60 prostate tumors and 16 non-tumor prostate tissues, tumor samples were found to have higher levels of miR-106b-25 cluster compared to non-tumor tissues (Ambs et al., 2008). Tumorigenic effects of miR-106b in prostate cancer was suggested to be exerted by targeting PTEN (phosphate and tensin homolog) - a tumor suppressor gene. PTEN inhibits the PI3K-Akt pathway which is a signal transduction pathway taking role in cell survival, proliferation, motility and angiogenesis (Poliseno et al., 2010). |
Entity | Hepatocellular carcinoma |
Note | 56 pairs of hepatocellular carcinoma (HCC) samples and corresponding non-tumor liver samples were analyzed and significant up-regulation of miR-106b was observed in tumor samples. Moreover in this study, decrease in the proliferation of two hepatoma-derived cell lines was shown after inhibiting miR-106b by an anti-miR-106b oligo. BCL2L11 (Bim) was identified as target of miR-106b and correlation between BCL2L11 (Bim) (pro-apoptotic gene) and miR-106b was shown in hepatocellular carcinoma. Bim expression was higher in tumors that have down regulated expression of miR-106b (Li et al., 2009). The same upregulated pattern of miR-106b was shown in the study of Shen et al. (2013), in which HCC cell lines and tissues were analyzed by quantitative RT-PCR in terms of miR-106b expression. It was depicted that miR-106b upregulation affected G1/S transition by upregulating cyclin D1 and downregulating adenomatous polyposis coli (APC) - an important tumor suppressor gene. APC was shown as a direct target of miR-106b in this study. |
Entity | Hepatocellular carcinoma (HCC) and hepatitis B virus (HBV) infection |
Note | A genetic variant (SNP A>G) in the promoter region of miR-106b-25 cluster suggested to provide a protective effect against HBV chronic infection. However, the polymorphism was also predicted to cause increased risk for HCC by increasing expression of miR-106b-25 cluster (Liu et al., 2012). |
Entity | Breast cancer |
Note | In a study conducted with 204 lymph node negative breast cancers, high expression of miR-106b was shown to be correlated with high proliferation and estrogen receptor positivity (Jonsdottir et al., 2012). The role of miR-106b-25 cluster in breast cancer was depicted with study of Smith and his colleagues. The relation between miR-106b-25, TGFβ and homeobox protein SIX1 (Six1) was studied. It was shown that miR-106b-25 cluster can target Smad-7 - a TGFβ inhibitor - and activate TGFβ pathway as a downstream effect of SIX1 overexpression. Hence, miR-106b-25 cluster overcomes TGFβ mediated growth suppression and also promote TGFβ pathway signaling in favor of tumorigenesis (Smith et al., 2012). Loss of membranous E-cadherin is known as one of the hallmarks for epithelial-to-mesenchymal transition (EMT). miR-106b-25 cluster overexpressing breast cancer cells had decreased membrane bound E-cadherin, which was in agreement with EMT (Smith et al., 2012). |
Entity | Laryngeal carcinoma |
Note | Inhibition of miR-106b by antisense oligonucleotides showed a decrease in proliferation of two laryngeal carcinoma cell lines and this inhibition resulted in G0/G1 arrest (Cai et al., 2011). Retinoblastoma protein (Rb), which is a tumor suppressor and has a role in G1/S transition, was shown as a direct target of miR-106b in laryngeal carcinoma. |
Entity | Glioma |
Note | miR-106b levels were assessed in 71 glioma samples and overexpression was observed in the majority of samples by in situ hybridization (ISH) and real-time PCR. Moreover, expression of miR-106b was found to be positively correlated with the tumor grade. After the transfection of antisense oligonucleotides for miR-106b in three human glioma cell lines, a decrease in the proliferation of these cells was observed. RBL2 (retinoblastoma like-2) was also shown to be target of miR-106b and miR-106b promoted cell cycle progression by negatively regulating RBL2 (Zhang et al., 2013). |
Entity | Alzheimer's disease (AD) |
Note | miR-106b levels were shown to be reduced in sporadic AD patients. Important role of TGFβ pathway has been implicated in AD pathogenesis (Tesseur et al., 2006; Caraci et al., 2011) and direct regulation of TGFβ receptor 2 (TGFBR2) by miR-106b was revealed. Hence, potential role of miR-106b in AD pathogenesis via affecting TGFβ pathway was suggested (Wang et al., 2010). |
Entity | Induced pluripotent stem cells (iPSC) |
Note | In iPSC, miR-106b-25 cluster is induced in early reprogramming phases and inhibition of this cluster reduces the reprogramming efficiency. miR-93 and miR-106b target TGFBR2 and CDKN1A (p21) which have already been linked to iPSC induction (Li et al., 2011). |
Bibliography |
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MiR-106b promotes cell proliferation via targeting RB in laryngeal carcinoma. |
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Citation |
This paper should be referenced as such : |
Saygili, C ; Erson-Bensan, AE |
MIR106B (microRNA 106b) |
Atlas Genet Cytogenet Oncol Haematol. 2013;17(12):821-824. |
Free journal version : [ pdf ] [ DOI ] |
External links |
REVIEW articles | automatic search in PubMed |
Last year publications | automatic search in PubMed |
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