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ZMYND10 (zinc finger, MYND-type containing 10)

Written2014-07Xiangning Zhang, Michael I Lerman, Zhiwei He
Guangdong Medical College, Dongguan, Guangdong 523808, China (XZ, ZH); Affina Biotechnologies, Inc., Stamford, CT USA (MIL)

Abstract The candidate tumor suppressor gene ZMYND10/BLU, is located on the minimal deleted fragment of 110 kb in chromosomal region 3p21.3. It was initially identified by PCR in search of the b-catenin homolog in lung cancer. BLU codes for a protein with 440 amino acid residues, which contains a zinc finger myelogenous nervy domain (zMYND) motif on its carboxyl terminus. The characteristic domain defines a ZMYNND protein family, some of its member have been found in the frequently affected region translocated during acute leukemias, and were described to be transcriptional repressors. BLU/ZMYND10 is inactivated in a variety of human tumors due to genetic or epigenetic mechanisms, but the function is largely unknown. It has been reported that similar with certain tumor suppressors, it donwregulates JNK/MAPK signaling to exert inhibition on growth and proliferation. ZMYND10 is implicated in the respiratory ciliary dyskinesia.

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HGNC Alias symbBLU
HGNC Alias namedynein axonemal assembly factor 7
LocusID (NCBI) 51364
Atlas_Id 45815
Location 3p21.31  [Link to chromosome band 3p21]
Location_base_pair Starts at 50341113 and ends at 50345732 bp from pter ( according to GRCh38/hg38-Dec_2013)  [Mapping ZMYND10.png]
Local_order Telomeric to NPRL2/G21, and centromeric to RASSF1.
Fusion genes
(updated 2017)
Data from Atlas, Mitelman, Cosmic Fusion, Fusion Cancer, TCGA fusion databases with official HUGO symbols (see references in chromosomal bands)


Note NM_015896, 4.7 kb.
  The gene of 4.5-4.7 kb contains 12 (lung version, termed as canonic) or 11 (testis version) exons coding for a 2-kb, alternatively spliced mRNA, well expressed in lung and testis but not expressed in all other tested human tissues.
Description The genomic size of the gene is about 4.5 kb.
Transcription The testis isoform contains 11 exons because of a complex selection of an alternative acceptor site.
Pseudogene No known pseudogenes.


Note NP_056980; ZMYND10 (zinc finger, myeloid, nervy and DEAF-1 (MYND)-type containing 10).
  See below.
Description The BLU protein is likely a soluble cytoplasmic protein and shares 30-32% identity over a stretch of 100-112 amino acids (residues 334-437 or 318-430) with proteins of the MTG/ETO family of transcription factors and the suppressins. The most notable feature of the protein is a C-terminal MYND domain, spanning residues 394-430. The MYND domain constitutes a protein-protein interaction surface that appears to allow these proteins to act as transcriptional co-repressors by association with a variety of chromatin remodelling and transcription.
Expression Low level expression in most human tissues.
Localisation A majority of its coding product is located in cytoplasma.
Function The function of BLU/ZMYND10 is unknown. As a MYND-containing protein BLU/ZMYND10 is most likely to be involved in important transcriptional regulation pathways. It has been reported that BLU regulate cell cycle progression through inhibition JNK signaling.
Homology Shares 30-32% identity over a stretch of 100-112 amino acids (residues 334-437 or 318-430) with proteins of the MTG/ETO family of transcription factors and the suppressins.


Note The lung isoform is regarded as canonic isoform. The testis-specific protein isoform contains a different amino acid sequence between residues 199 and 234 as compared with the canonic lung-specific isoform. Mutation of BLU/ZMYND10 within a given isoform is a rare event in lung cancer and other cancers since missense changes were detected in only 3/61 lung tumour-cell lines. The eight-gene set in the 120-kb region show that the mutation rate was in the range of 5%. Missense mutations were discovered in a sample of 61 lung cancer cell lines. It has been shown that, however, mutated ZMYND10 protein carrying substitution of some amino acid residues binds LRRC6 and contributes to pathogenesis of primary ciliary dyskinesia (PCD, or CILD22).
Somatic Mutation carried by testis isoform 200-234: SLSLSTLSRMLSTHNLPCLLVELLEHSPWSRREGG → RQWSVSQPPQLAHLKRIQRLHPVCWFLSPG; results in the loss of one of three PKC phosphorylation sites (residues 229-231). The substitutions documented in PCD include: ZMYND10, VAL16GLY, SER29PRO, LEU39PRO, LEU266PRO, ARG369TRP, Tyr379CYS, and ASP198GLN, ARG407GLU in non-small cell lung cancer cells.

Implicated in

Entity Various cancers
Note The gene codes for the putative tumor suppressor BLU is primarily expressed in the lung and testis, as tissue-specific isoforms, but the level is low in other tissues. The expression is varied in lung cancer cells, but a non-small lung cancer line, A549 has high level of BLU. A majority of nasopharyngeal carcinoma-derived cell lines, however, has downregulated expression of BLU. Mutation of the gene is relatively rare. Hypermethylation on BLU promoter has been detected ranging from 19% of primary non-small cell lung cancer to 66-74% of nasopharyngeal carcinoma (NPC).
Disease Mutated BLU/ZMYND10 protein with several amino acid residues substitution has been shown to associate with LRRC6, and plays a role in the pathogenesis of primary ciliary dyskinesia. Hypermethylation and downregulation has been described as a frequent event in primary tumours such as glioma (80%), cervical squamous cell carcinomas (77%), NPC (66%), neuroblastoma (41-70%) and NSCLC (19-43%) with lower frequencies observed in gallbladder carcinomas (26%), ependymomas (13.6%) and SCLC (14%). It has been noted that in some tumors like glioma, methylation of BLU is an early detectable event; it was identified in stage II glioma and stage I/II cervical squamous cell carcinomas.
Cytogenetics Unlike translocation frequently seen in acute myelogenous leukemia, involving ZMYND motif containing MTG8, no cytogenetic anomaly affecting BLU has been observed in malignancies.
Hybrid/Mutated Gene No fusion gene(s) involving BLU has been reported.
Entity Lung cancer
Note BLU is primarily expressed in lung and testis, with different isoforms. The mutation is rare. The expression is absent in a number of lung cancer cell lines, and in 19-43% of non-small lung cancer (NSLC) cases, BLU is silenced due to promoter hypermethylation (Agathanggelou et al., 2003; Marsit et al., 2005). The incidence is higher in adenocarcinoma (AC) than in squamous cell carcinoma (SCC). Frequent methylation for BLU and RASSF1 has been observed but there is no significant association. In lung cancer patients, homozygous deletion of 3p21 region has been association with early age of cigarette smoking initiation.
Entity Nasopharyngeal carcinoma (NPC)
Note Downregulation of BLU expression was well correlated with the promoter hypermethylation in tumor specimens and cultured cell lines. Methylation on BLU promoter was identified in up to 66% of the tumors, and 6 out 7 passaged cell lines. BLU was observed to inhibit JNK signaling pathway, and cyclin D1 (CCND1) gene promoter activity, arrest cell cycle at G1 phase, and block in vitro and in vivo NPC cell growth.
Entity Glioma
Note BLU/ZMYND10 hypermethylation and downregulation has been described as a frequent event in up to 80% primary tumours of glioma. BLU/ZMYND10 methylation is an early event detectable in stage II glioma (Hesson et al., 2004). In glioma tumours methylation of BLU/ZMYND10 and/or RASSF1A, located adjacent to BLU/ZMYND10, was detected in more than 95% (52/54) primary tumours.
Entity Neuroblastoma
Note Methylation leading to downregulation of BLU has been described in up to 70% neuroblastoma (41-70%) (Abe et al., 2005). It was shown that methylation of promoter CGIs of RASSF1A (3p21) and BLU (3p21) was far more frequently observed in neuroblastomas with CpG island methylator phenotype (CIMP).
Entity Esophageal cancer
Note In esophageal squamous cell carcinoma (ESCC), BLU expression was downregulated in three out of four Asian esophageal carcinoma cell lines, and 4 out of 8 pairs of tumor and normal tissues. Methylation specific-PCR revealed the down-regulation of BLU by epigenetic inactivation. However, exogenous expression of BLU did not functionally suppress tumorigenicity in nude mice. These results suggest that over-expression of BLU alone is not sufficient to inhibit tumorigenicity. (Yi Lo et al., 2006).
Entity Ovarian carcinoma
Note Epithelial ovarian carcinoma is usually present at the advanced stage, during which the patients generally have poor prognosis. Our study aimed to evaluate the correlation of gene methylation and the clinical outcome of patients with advanced-stage, high-grade ovarian serous carcinoma. The methylation status of eight candidate genes was first evaluated by methylation-specific PCR and capillary electrophoresis to select three potential genes including DAPK, CDH1, and BLU (ZMYND10) from the exercise group of 40 patients. The methylation status of these three genes was further investigated in the validation group consisting of 136 patients. Patients with methylated BLU had significantly shorter progression-free survival (PFS; hazard ratio (HR) 1.48, 95% CI 1.01-2.56, P=0.013) and overall survival (OS; HR 1.83, 95% CI 1.07-3.11, P=0.027) in the multivariate analysis. Methylation of BLU was also an independent risk factor for 58 patients undergoing optimal debulking surgery for PFS (HR 2.37, 95% CI 1.03-5.42, P=0.043) and OS (HR 3.96, 95% CI 1.45-10.81, P=0.007) in the multivariate analysis. A possible mechanism of BLU in chemoresistance was investigated in ovarian cancer cell lines by in vitro apoptotic assays. In vitro studies have shown that BLU could upregulate the expression of BAX and enhance the effect of paclitaxel-induced apoptosis in ovarian cancer cells. Our study suggested that methylation of BLU could be a potential prognostic biomarker for advanced ovarian serous carcinoma.
Prognosis Its correlation with prognosis of serous ovarian carcinoma has been documented. The methylation status of eight candidate genes, including BLU was first evaluated by methylation-specific PCR and capillary electrophoresis from tumor tissues of ovarian carcinoma in a group of patients. Patients with methylated BLU had significantly shorter progression-free survival and overall survival in the multivariate analysis (Chiang et al., 2013).
Entity Myelodysplastic syndrome (MDS)
Note Hypermethylation in the promoter region and downregulation at mRNA and protein levels of BLU was detected in 34 of 79 (43%) MDS patient samples. There was a statistically significant difference in methylation frequency between different refractory anemia groups. The demethylating agent decitabine could partly reverse hypermethylation and restore the expression of the BLU gene. BLU promoter hypermethylation frequently occurs in higher risk MDS cases. BLU may play a role in the development and etiology of MDS.
Entity Primary ciliary dyskinesia (PCD)
Note ZMYND10 bound to LRRC6 in HEK293T and in human tracheal epithelial cells. These two proteins localized to both the basal body and the striated rootlet in Xenopus ciliated epithelial cells. The C-terminal MYND domain of ZMYND10 was insufficient for interaction with the CS domain of LRRC6; but a C-terminal fragment expanding 366-440 amino acids extending beyond the MYND domain was necessary for interaction (see the scheme of protein diagram). Similar studies using progressive truncating constructs of LRRC6 confirmed that the C-terminal CS domain of LRRC6 is sufficient for the binding with ZMYND10. The protein-protein interaction is abrogated by truncating mutations in either gene in patients with CILD.


CpG island methylator phenotype is a strong determinant of poor prognosis in neuroblastomas.
Abe M, Ohira M, Kaneda A, Yagi Y, Yamamoto S, Kitano Y, Takato T, Nakagawara A, Ushijima T.
Cancer Res. 2005 Feb 1;65(3):828-34.
PMID 15705880
Epigenetic inactivation of the candidate 3p21.3 suppressor gene BLU in human cancers.
Agathanggelou A, Dallol A, Zochbauer-Muller S, Morrissey C, Honorio S, Hesson L, Martinsson T, Fong KM, Kuo MJ, Yuen PW, Maher ER, Minna JD, Latif F.
Oncogene. 2003 Mar 13;22(10):1580-8.
PMID 12629521
Tumor suppressor genes on frequently deleted chromosome 3p in nasopharyngeal carcinoma.
Chen J, Fu L, Zhang LY, Kwong DL, Yan L, Guan XY.
Chin J Cancer. 2012 May;31(5):215-22. doi: 10.5732/cjc.011.10364. Epub 2012 Feb 24. (REVIEW)
PMID 22360856
Epigenetic silencing of BLU through interfering apoptosis results in chemoresistance and poor prognosis of ovarian serous carcinoma patients.
Chiang YC, Chang MC, Chen PJ, Wu MM, Hsieh CY, Cheng WF, Chen CA.
Endocr Relat Cancer. 2013 Mar 22;20(2):213-27. doi: 10.1530/ERC-12-0117. Print 2013 Apr.
PMID 23329649
Frequent epigenetic inactivation of RASSF1A and BLU genes located within the critical 3p21.3 region in gliomas.
Hesson L, Bieche I, Krex D, Criniere E, Hoang-Xuan K, Maher ER, Latif F.
Oncogene. 2004 Mar 25;23(13):2408-19.
PMID 14743209
Expression of several genes in the human chromosome 3p21.3 homozygous deletion region by an adenovirus vector results in tumor suppressor activities in vitro and in vivo.
Ji L, Nishizaki M, Gao B, Burbee D, Kondo M, Kamibayashi C, Xu K, Yen N, Atkinson EN, Fang B, Lerman MI, Roth JA, Minna JD.
Cancer Res. 2002 May 1;62(9):2715-20.
PMID 11980673
Molecular cloning, sequence analysis, expression, and tissue distribution of suppressin, a novel suppressor of cell cycle entry.
LeBoeuf RD, Ban EM, Green MM, Stone AS, Propst SM, Blalock JE, Tauber JD.
J Biol Chem. 1998 Jan 2;273(1):361-8.
PMID 9417089
The 630-kb lung cancer homozygous deletion region on human chromosome 3p21.3: identification and evaluation of the resident candidate tumor suppressor genes. The International Lung Cancer Chromosome 3p21.3 Tumor Suppressor Gene Consortium.
Lerman MI, Minna JD.
Cancer Res. 2000 Nov 1;60(21):6116-33.
PMID 11085536
Alterations of BLU, a candidate tumor suppressor gene on chromosome 3p21.3, in human nasopharyngeal carcinoma.
Liu XQ, Chen HK, Zhang XS, Pan ZG, Li A, Feng QS, Long QX, Wang XZ, Zeng YX.
Int J Cancer. 2003 Aug 10;106(1):60-5.
PMID 12794757
Hypermethylation of RASSF1A and BLU tumor suppressor genes in non-small cell lung cancer: implications for tobacco smoking during adolescence.
Marsit CJ, Kim DH, Liu M, Hinds PW, Wiencke JK, Nelson HH, Kelsey KT.
Int J Cancer. 2005 Mar 20;114(2):219-23.
PMID 15540210
Tumor suppressor BLU promotes paclitaxel antitumor activity by inducing apoptosis through the down-regulation of Bcl-2 expression in tumorigenesis.
Park ST, Byun HJ, Kim BR, Dong SM, Park SH, Jang PR, Rho SB.
Biochem Biophys Res Commun. 2013 May 24;435(1):153-9. doi: 10.1016/j.bbrc.2013.04.061. Epub 2013 Apr 27.
PMID 23628417
The candidate tumor suppressor gene BLU, located at the commonly deleted region 3p21.3, is an E2F-regulated, stress-responsive gene and inactivated by both epigenetic and genetic mechanisms in nasopharyngeal carcinoma.
Qiu GH, Tan LK, Loh KS, Lim CY, Srivastava G, Tsai ST, Tsao SW, Tao Q.
Oncogene. 2004 Jun 10;23(27):4793-806.
PMID 15122337
Frequent epigenetic inactivation of chromosome 3p candidate tumor suppressor genes in gallbladder carcinoma.
Riquelme E, Tang M, Baez S, Diaz A, Pruyas M, Wistuba II, Corvalan A.
Cancer Lett. 2007 May 18;250(1):100-6. Epub 2006 Nov 7.
PMID 17084965
Structure and expression of the human MTG8/ETO gene.
Wolford JK, Prochazka M.
Gene. 1998 May 28;212(1):103-9.
PMID 9661669
Tumor suppressor gene BLU is frequently downregulated by promoter hypermethylation in myelodysplastic syndrome.
Yang Y, Zhang Q, Xu F, Wu L, He Q, Li X.
J Cancer Res Clin Oncol. 2012 May;138(5):729-37. doi: 10.1007/s00432-012-1151-0. Epub 2012 Jan 15.
PMID 22246278
Expression of candidate chromosome 3p21.3 tumor suppressor genes and down-regulation of BLU in some esophageal squamous cell carcinomas.
Yi Lo PH, Chung Leung AC, Xiong W, Law S, Duh FM, Lerman MI, Stanbridge EJ, Lung ML.
Cancer Lett. 2006 Mar 28;234(2):184-92.
PMID 15885884
Tumor suppressor BLU inhibits proliferation of nasopharyngeal carcinoma cells by regulation of cell cycle, c-Jun N-terminal kinase and the cyclin D1 promoter.
Zhang X, Liu H, Li B, Huang P, Shao J, He Z.
BMC Cancer. 2012 Jun 22;12:267. doi: 10.1186/1471-2407-12-267.
PMID 22727408


This paper should be referenced as such :
Xiangning Zhang, Michael I Lerman, Zhiwei He
ZMYND10 (zinc finger, MYND-type containing 10)
Atlas Genet Cytogenet Oncol Haematol. 2015;19(5):319-323.
Free journal version : [ pdf ]   [ DOI ]

External links


HGNC (Hugo)ZMYND10   19412
Entrez_Gene (NCBI)ZMYND10    zinc finger MYND-type containing 10
GeneCards (Weizmann)ZMYND10
Ensembl hg19 (Hinxton)ENSG00000004838 [Gene_View]
Ensembl hg38 (Hinxton)ENSG00000004838 [Gene_View]  ENSG00000004838 [Sequence]  chr3:50341113-50345732 [Contig_View]  ZMYND10 [Vega]
ICGC DataPortalENSG00000004838
TCGA cBioPortalZMYND10
Genatlas (Paris)ZMYND10
SOURCE (Princeton)ZMYND10
Genetics Home Reference (NIH)ZMYND10
Genomic and cartography
GoldenPath hg38 (UCSC)ZMYND10  -     chr3:50341113-50345732 -  3p21.31   [Description]    (hg38-Dec_2013)
GoldenPath hg19 (UCSC)ZMYND10  -     3p21.31   [Description]    (hg19-Feb_2009)
GoldenPathZMYND10 - 3p21.31 [CytoView hg19]  ZMYND10 - 3p21.31 [CytoView hg38]
Genome Data Viewer NCBIZMYND10 [Mapview hg19]  
OMIM607070   615444   
Gene and transcription
Genbank (Entrez)AB209621 AK058135 AK093455 AK096525 AK223343
RefSeq transcript (Entrez)NM_001308379 NM_015896
Consensus coding sequences : CCDS (NCBI)ZMYND10
Gene ExpressionZMYND10 [ NCBI-GEO ]   ZMYND10 [ EBI - ARRAY_EXPRESS ]   ZMYND10 [ SEEK ]   ZMYND10 [ MEM ]
Gene Expression Viewer (FireBrowse)ZMYND10 [ Firebrowse - Broad ]
GenevisibleExpression of ZMYND10 in : [tissues]  [cell-lines]  [cancer]  [perturbations]  
BioGPS (Tissue expression)51364
GTEX Portal (Tissue expression)ZMYND10
Human Protein AtlasENSG00000004838-ZMYND10 [pathology]   [cell]   [tissue]
Protein : pattern, domain, 3D structure
UniProt/SwissProtO75800   [function]  [subcellular_location]  [family_and_domains]  [pathology_and_biotech]  [ptm_processing]  [expression]  [interaction]
NextProtO75800  [Sequence]  [Exons]  [Medical]  [Publications]
With graphics : InterProO75800
Domaine pattern : Prosite (Expaxy)ZF_MYND_1 (PS01360)    ZF_MYND_2 (PS50865)   
Domains : Interpro (EBI)UCP037948_Znf-MYND    Znf_MYND   
Domain families : Pfam (Sanger)zf-MYND (PF01753)   
Domain families : Pfam (NCBI)pfam01753   
Conserved Domain (NCBI)ZMYND10
PDB (RSDB)2D8Q    2DAN   
PDB Europe2D8Q    2DAN   
PDB (PDBSum)2D8Q    2DAN   
PDB (IMB)2D8Q    2DAN   
Structural Biology KnowledgeBase2D8Q    2DAN   
SCOP (Structural Classification of Proteins)2D8Q    2DAN   
CATH (Classification of proteins structures)2D8Q    2DAN   
AlphaFold pdb e-kbO75800   
Human Protein Atlas [tissue]ENSG00000004838-ZMYND10 [tissue]
Protein Interaction databases
IntAct (EBI)O75800
Ontologies - Pathways
Ontology : AmiGOcilium movement  protein binding  cytoplasm  cytoplasm  protein folding  apical plasma membrane  centriolar satellite  centriolar satellite  outer dynein arm assembly  outer dynein arm assembly  outer dynein arm assembly  inner dynein arm assembly  inner dynein arm assembly  inner dynein arm assembly  protein folding chaperone  motile cilium assembly  motile cilium assembly  metal ion binding  molecular adaptor activity  protein localization to cilium  dynein axonemal particle  positive regulation of motile cilium assembly  
Ontology : EGO-EBIcilium movement  protein binding  cytoplasm  cytoplasm  protein folding  apical plasma membrane  centriolar satellite  centriolar satellite  outer dynein arm assembly  outer dynein arm assembly  outer dynein arm assembly  inner dynein arm assembly  inner dynein arm assembly  inner dynein arm assembly  protein folding chaperone  motile cilium assembly  motile cilium assembly  metal ion binding  molecular adaptor activity  protein localization to cilium  dynein axonemal particle  positive regulation of motile cilium assembly  
NDEx NetworkZMYND10
Atlas of Cancer Signalling NetworkZMYND10
Wikipedia pathwaysZMYND10
Orthology - Evolution
GeneTree (enSembl)ENSG00000004838
Phylogenetic Trees/Animal Genes : TreeFamZMYND10
Homologs : HomoloGeneZMYND10
Homology/Alignments : Family Browser (UCSC)ZMYND10
Gene fusions - Rearrangements
Fusion : QuiverZMYND10
Polymorphisms : SNP and Copy number variants
NCBI Variation ViewerZMYND10 [hg38]
dbSNP Single Nucleotide Polymorphism (NCBI)ZMYND10
Exome Variant ServerZMYND10
GNOMAD BrowserENSG00000004838
Varsome BrowserZMYND10
ACMGZMYND10 variants
Genomic Variants (DGV)ZMYND10 [DGVbeta]
DECIPHERZMYND10 [patients]   [syndromes]   [variants]   [genes]  
CONAN: Copy Number AnalysisZMYND10 
ICGC Data PortalZMYND10 
TCGA Data PortalZMYND10 
Broad Tumor PortalZMYND10
OASIS PortalZMYND10 [ Somatic mutations - Copy number]
Somatic Mutations in Cancer : COSMICZMYND10  [overview]  [genome browser]  [tissue]  [distribution]  
Somatic Mutations in Cancer : COSMIC3DZMYND10
Mutations and Diseases : HGMDZMYND10
LOVD (Leiden Open Variation Database)[gene] [transcripts] [variants]
DgiDB (Drug Gene Interaction Database)ZMYND10
DoCM (Curated mutations)ZMYND10
CIViC (Clinical Interpretations of Variants in Cancer)ZMYND10
NCG (London)ZMYND10
Impact of mutations[PolyPhen2] [Provean] [Buck Institute : MutDB] [Mutation Assessor] [Mutanalyser]
OMIM607070    615444   
Genetic Testing Registry ZMYND10
NextProtO75800 [Medical]
Target ValidationZMYND10
Huge Navigator ZMYND10 [HugePedia]
Clinical trials, drugs, therapy
Protein Interactions : CTDZMYND10
Pharm GKB GenePA134981649
Clinical trialZMYND10
DataMed IndexZMYND10
PubMed53 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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