|Written||2014-02||Alfons Navarro, Marina Díaz-Beyá, Mariano Monzó|
|Molecular Oncology, Embryology Laboratory, Human Anatomy Unit, School of Medicine, University of Barcelona, Barcelona, Spain (AN, MM); Hematology Department, Hospital Clinic, IDIBAPS, Barcelona, Spain (MDB)|
|Location||3p21.1 [Link to chromosome band 3p21]|
|Location_base_pair||Starts at 52294219 and ends at 52294308 bp from pter ( according to hg19-Feb_2009) [Mapping MIR135A1.png]|
|Local_order||Genes flanking MIR135A1 oriented from centromere to telomere on 3p21.1:
- PHF7: PHD finger protein 7, 3p21.1
- BAP1: BRCA1 associated protein-1 (ubiquitin carboxy-terminal hydrolase), 3p21.31-p21.2
- DNAH1: dynein, axonemal, heavy chain 1, 3p21.1
- GLYCTK-AS1: GLYCTK Antisense RNA 1 (Non-protein coding), 3p21.1
- GLYCTK: glycerate kinase, 3p21.1
- TCONS_00006853; lnc-GLYCTK-1, 3p21.1
- WDR82: WD repeat domain 82, 3p21.2
- MIRLET7G: microRNA let-7g, 3p21.1.
|A. Stem-loop structure of hsa-mir-135a-1. B. Genomic location of MIR135A 1 and its host genes.|
|Description||The gene is located in the intron 1 of GLYCTK-AS1/RP11 gene (sense) and in the exon 4 of GLYCTK (antisense). The precursor length is 90 nt.|
|Transcription|| The transcription of miR-135a is regulated by FOXM1 in hepatocellular carcinoma (Liu et al., 2012). |
BMP2 inhibits miR-135a expression during osteoblast differentiation (Li et al., 2008).
|Pseudogene||No reported pseudogenes.|
|Note||MicroRNAs are not translated into amino acids.|
|Note||Deletions of miR-135a-1 gene have been described in medulloblastomas, where 16/48 (33%) of medulloblastoma patients had a deletion of miR-135a-1 gene (Lv et al., 2012).|
|Entity||Colorectal cancer (CRC)|
|Note||Interestingly, treating CRC cell lines with mistletoe lecitin-I, degrades precursor of some microRNAs, including pre-mir-135a, thus dowregulating miR-135 and upregulating APC and increasing beta-catenin phosphorylation (Li et al., 2011).|
|Prognosis||A prognostic miRNA signature composed of miR-135a, miR-21, miR-335, miR-206 and let-7a was useful to detect the presence of metastasis (Vickers et al., 2012).|
|Oncogenesis|| Oncogene. |
miRNA expression: Overexpression among colorectal adenome and carcinome in comparison with normal tissue. miR-135 family (miR-135a and miR-135b) overexpression during CRC progression (in patients) (Nagel et al., 2008). Consistently, a study comparing patient samples, healthy controls and cell lines showed overexpression in CRC samples (Zhou et al., 2012). Another study also showed overexpression associated with progression and metastasis (Vickers et al., 2012).
Targets: Adenomatous polyposis coli (APC) (Nagel et al., 2008). Metastasis suppressor 1 (MTSS1) (Zhou et al., 2012).
Function: miR-135a and miR-135b inhibits APC translation (independently of mutational status of APC) activating downstream Wnt pathway activity and induce beta-catenin signaling (Nagel et al., 2008). In CRC cell lines, miR-135a overexpression increased proliferation and promoted mobility and invasion in part by targeting MTSS1 (Zhou et al., 2012).
|Oncogenesis|| Tumor suppressor (Wu H et al., 2012). |
miRNA expression: Downregulation in gastric cancer patient samples in comparison with adjacent normal tissue.
Targets: JAK2 (Janus kinase 2)
Function: miR-135a overexpression produces downregulation of JAK2 levels reducing cell proliferation and colony formation. It also reduces p-STAT3 (phospho signal transducer and activator of transcription 3) activation and cyclin D1 and Bcl-x (BCL2-like1).
|Entity||Hepatocellular carcinoma (HCC)|
|Prognosis||In a cohort of 50 patients, overexpression of miR-135a identified a group of patients with worse OS end DFS among patients with PVTT.|
|Oncogenesis|| Oncogene (Liu et al., 2012). |
miRNA expression: Overexpression of miR-135a in samples from HCC with portal vein tumor thrombus (PVTT) - that is considered a special type of HCC metastasis - compared with parenchyma tumor nodes.
Function: miR-135a promotes invasion and metastasis in vitro and in mouse models of HCC. Reducing miR-135a leads to reduced PVTT. The transcription of miR-135a is regulated by FOXM1.
|Oncogenesis|| Oncogene (Chen et al., 2012). |
miRNA expression: Overexpression in metastasic breast tumors in comparison with benign tumor patient samples. Upregulation in the highly invasive breast cancer cell line BT 549 in comparison with other breast cancer cell lines.
Targets: HOXA10 (homeobox A10).
Function: miR-135a promotes the migration and invasion of breast cancer cells at least in part through HOXA10.
|Oncogenesis|| Tumor suppressor (Wu S et al., 2012). |
miRNA expression: Downregulated in glioma in comparison with normal glia. miRNA-135a correlated negatively with the pathological grading of human glioma tissue samples.
Targets: STAT6 (signal transducer and activator of transcription 6), SMAD5 (SMAD family member 5), BMPR2 (bone morphogenetic protein receptor, type II).
Function: miR-135a selectively induces mitochondria-dependent apoptosis of malignant glioma by targeting various genes (STAT6, SMAD5, BMPR2). Interestingly it doesn't affect normal glia cells.
|Oncogenesis|| Tumor suppressor (Cheng et al., 2013; Zhou et al., 2013). |
miRNA expression: miR-135a/b downregulated in the cisplatin-resistant cell line A549R compared with the cisplatin-sensitive A549 cell line (Zhou, Qiu et al. 2013)
Targets: MCL1 (myeloid cell leukemia sequence 1) (Zhou et al., 2013), CD133 (Cheng et al., 2013).
Function: Overexpression of miR-135a/b reduced MCL1 and sensitized cell lines to cisplatin by modulation of apoptosis (Zhou et al., 2013). miR-135a/b suppressed CD133 only in CD133 with binding polymorphism rs2240688 CC or CA but not in genotype AA (Cheng et al., 2013).
|Entity||Classic Hodgkin lymphoma (cHL)|
|Prognosis||In a cohort of 89 cHL patients, low miR-135a was associated with a higher risk of relapse and worse disease free survival.|
|Oncogenesis|| Tumor suppressor (Navarro et al., 2008; Navarro et al., 2009). |
miRNA expression: Downregulated miR-135a in cHL patient lymph nodes in comparison with reactive non-tumor lymph nodes used as control.
Function: Overexpression of miR-135a increases apoptosis and decreases cellular growth in HL cell lines through regulation of JAK/STAT pathway and activation BcL-xL expression.
|Entity||Acute myeloid leukemia (AML)|
|Prognosis||In a cohort of 85 intermediate risk AML (IR-AML) patients (later extended to 238 IR-AML patients), low expression of miR-135a identified a group of patients with a higher risk of relapse - both in the entire cohort and also within the unfavourable molecular subgroup (FLT3-ITD or wild-type NPM and CEBPA) (Díaz-Beyá et al., 2014).|
|Entity||Renal cell carcinoma|
|Oncogenesis|| Tumor suppressor (Hidaka et al., 2012). |
miRNA expression: Lower expression of miR-135a observed in 10 cancer tissue samples compared to 5 adjacent non-cancer tissue samples.
Function: Effect on cell proliferation, where the miR-135a overexpression reduces cell viavility.
|Entity||Cervival cancer cell|
|Oncogenesis|| Oncogene (Leung et al., 2014). |
miRNA expression: miR-135a is overexpressed in cervical squamous cell carcinoma in comparison with cervical intraepithelial neoplasia (precancerous lesions).
Targets: SIAH1 (in cervical cancer cells and cervical epithelial cells).
Function: Overexpression of miR-135a induced increased colony formation, anchorage-independent growth, and proliferation, cell-invasion and migration in cervical cancer cell lines. The inhibition of miR-135a on SIAH1 led to upregulation of beta-catenin activity, indicating that miR-135a induces transformation and enhances tumor growth. The authors analyzed the miR-135a-induced malignant transformation activity in cell lines with or without human papiloma virus (HPV) proteins (E6 and E7) and concluded that these proteins are necessary for miR-135a oncogenic activity. Also in xenografts, miR-135a improved the growth of cancer cells and the tumorigenic activity of HPV cells.
|Entity||Various tumor cell lines (HeLa cervical carcinoma, SW480 colon cancer, A375 melanoma, PANC-1 pancreatic tumor, and 293 epithelial kidney cells)|
|Note||FAK is overexpressed in many cancers.|
|Oncogenesis|| Tumor suppressor (Golubovskaya et al., 2014). |
Targets: FAK (focal adhesion kinase).
Function: miR-135a overexpression decreased FAK mRNA and protein levels, decreased cell invasion and increased sensitivity to doxorubicin, 5-fluorouacil and FAK inhibitor Y15.
|Entity||Various tumor cell lines|
|Oncogenesis|| Oncogene (Holleman et al., 2011). |
miRNA expression: miR-135a levels were significantly upregulated in paclitaxel-resistant ovarian, lung, uterine, breast and prostate tumor cells lines derived from A549, PC-14, MCF-7, PC-3, SKOV-3 and MES-SA.
Function: miR-135a upregulation in vitro and in vivo is associated with paclitaxel resistance. Anti-miR-135a treatment in paclitaxel-resistant lung cancer xenografts restored sensitivity to paclitaxel, in part through the direct inhibition of APC expression.
|Note|| miRNA expression: Overexpression in diabetic human and mouse skeletal muscle. |
Targets: IRS2 (insulin receptor substrate 2).
Function: miR-135a inhibits IRS2, thus reducing glucose uptake into the cell. miR-135a overexpression attenuates insulin signaling and glucose uptake in skeletal muscle. In vivo, silencing miR-135a decreases hyperglicemia (Agarwal et al., 2013).
|Entity||Essential hypertension, renin-angiotensin-aldosteron system|
|Note|| Targets: NR3C2 (mineral corticoid receptor). |
Function: In Hela cells, overexpression of miR-135a and miR-124 downregulates NR3C2 protein, indicating a role in the regulation of blood pressure (Sõber et al., 2010).
|Entity||Corticoid dependent stress response|
|Note|| Targets: NR3C2 (mineral corticoid receptor, other alias MR) |
Function: In a mouse model, downregulation of miR-135a and miR-124 in amygdale after two hours of stress stimulus. Stress reaction by activation of corticosteroid signaling through NR3C2R. miR-135a and miR-124 are thus important components of the stress signaling response in the brain (Mannironi et al., 2013).
|Entity||Development, congenital disease and others|
|Note|| miRNA expression: In rat models, low expression of miR-135a in undescended testis in comparison with that in contralateral normal testis. Higher miR-135a expression in the testes than in other organs. miR-135a is detected in spermatogonial stem cells.|
Targets: FoxO1 (forehead box protein O1).
Functions: miR-135a contributes to spermatogonial stem cell maintenance through modulation of FoxO1 (Moritoki et al., 2014).
|Note|| miRNA expression: Overexpressed in endometriosis in comparison with normal endometrial tissue (50 controls and 32 women with endometriosis). |
Targets: HOXA10 (homeobox A10).
Function: miR135a expression in controls was increased during the proliferative phase, decreased at the time of ovulation, and increased during the luteal phase (Petracco et al., 2011).
|Note|| miRNA expression: Very low levels in differentiated osteoblast, downregulated during BMP2-mediated osteogenic differentiation. |
Function: miR-135a suppresses osteogenesis and inhibits differentiation of osteoprogenitors and the osteogenic phenotype in pluripotent cells by attenuating SMAD5. BMP2 inhibits miR-135a expression and permits osteoblast differentiation (Li et al., 2008).
|Entity||Muscle differentiation (myogenesis) and Duchenne muscular dystrophy (DMD)|
|Note|| miRNA expression: miR-135a is upregulated during myogenic differentiation. Overexpression of miR-135a is observed when the myoblasts are differentiated in human samples, cell lines and mouse model (Greco et al., 2009). miR-135a is part of the DMD miRNA signature (Greco et al., 2009) and is overexpressed in Duchenne muscle (Cesana et al., 2011). |
Targets: MEF2C (myocyte enhancer factor 2C) (Cesana et al., 2011).
Function: Critical in myogenesis by targeting MEF2C. miR-135a inhibits MEF2C, leading to inhibition of muscle genes. LincRNA MD1 sponges miR-135a, allowing transcription of muscle genes. LincRNA MD1 is reduced in Duchenne muscle cells, so miR-135a is overexpressed and MEFC2 is downregulated (Cesana et al., 2011).
|Entity||Preimplantation embryo development|
|Note|| miRNA expression: Overexpressed in mouse zygote and decreased thereafter, indicating that it is a zygote-specific miRNA. |
Targets: SIAH1A (E3 ubiquitin ligase seven in absentia homolog 1A).
Function: miR-135a modulates the first cell cleavage through regulation of Siah1a. When miR-135a is inhibited, first cell cleavage is suppressed. mir-135a regulates proteosomal degradation (Pang et al., 2011).
|Entity||Mouse embryonic stem cells|
|Note|| miRNA expression: Upregulated during mouse embryonic stem cell differentiation. |
Targets: SIRT1 (sirtuin 1).
Function: Together with miR-181a, miR-181b, miR-9, miR-204 and miR-199b, miR-135a suppressed SIRT1 protein expression during mouse embryonic stem cell differentiation (Saunders et al., 2010).
|Entity||Bovine blastocyst development|
|Note||miRNA expression: miR-135a is part of a downregulated miRNA signature in more mature stage (Goossens et al., 2013).|
|Note||miRNA expression: A comparison between differentiated megakaryocytes with AML megakaryocytic cell lines found miR-135a higher in AML samples (Garzon et al., 2006).|
|Note|| miRNA expression: Downregulation of miR-135a (and miR199a-5p) in response to hypoxia. |
Targets: FLAP (5-lipoxygenase activating protein) (Gonsalves and Kalra, 2010).
|miR-135a targets IRS2 and regulates insulin signaling and glucose uptake in the diabetic gastrocnemius skeletal muscle.|
|Agarwal P, Srivastava R, Srivastava AK, Ali S, Datta M.|
|Biochim Biophys Acta. 2013 Aug;1832(8):1294-303. doi: 10.1016/j.bbadis.2013.03.021. Epub 2013 Apr 8.|
|A long noncoding RNA controls muscle differentiation by functioning as a competing endogenous RNA.|
|Cesana M, Cacchiarelli D, Legnini I, Santini T, Sthandier O, Chinappi M, Tramontano A, Bozzoni I.|
|Cell. 2011 Oct 14;147(2):358-69. doi: 10.1016/j.cell.2011.09.028.|
|miRNA-135a promotes breast cancer cell migration and invasion by targeting HOXA10.|
|Chen Y, Zhang J, Wang H, Zhao J, Xu C, Du Y, Luo X, Zheng F, Liu R, Zhang H, Ma D.|
|BMC Cancer. 2012 Mar 23;12:111. doi: 10.1186/1471-2407-12-111.|
|A microRNA-135a/b binding polymorphism in CD133 confers decreased risk and favorable prognosis of lung cancer in Chinese by reducing CD133 expression.|
|Cheng M, Yang L, Yang R, Yang X, Deng J, Yu B, Huang D, Zhang S, Wang H, Qiu F, Zhou Y, Lu J.|
|Carcinogenesis. 2013 Oct;34(10):2292-9. doi: 10.1093/carcin/bgt181. Epub 2013 May 28.|
|MicroRNA expression at diagnosis adds relevant prognostic information to molecular categorization in patients with intermediate-risk cytogenetic acute myeloid leukemia.|
|Diaz-Beya M, Brunet S, Nomdedeu J, Tejero R, Diaz T, Pratcorona M, Tormo M, Ribera JM, Escoda L, Duarte R, Gallardo D, Heras I, Queipo de Llano MP, Bargay J, Monzo M, Sierra J, Navarro A, Esteve J.|
|Leukemia. 2014 Apr;28(4):804-12. doi: 10.1038/leu.2013.281. Epub 2013 Sep 27.|
|MicroRNA fingerprints during human megakaryocytopoiesis.|
|Garzon R, Pichiorri F, Palumbo T, Iuliano R, Cimmino A, Aqeilan R, Volinia S, Bhatt D, Alder H, Marcucci G, Calin GA, Liu CG, Bloomfield CD, Andreeff M, Croce CM.|
|Proc Natl Acad Sci U S A. 2006 Mar 28;103(13):5078-83. Epub 2006 Mar 20.|
|MiR-138 and MiR-135 directly target focal adhesion kinase, inhibit cell invasion, and increase sensitivity to chemotherapy in cancer cells.|
|Golubovskaya VM, Sumbler B, Ho B, Yemma M, Cance WG.|
|Anticancer Agents Med Chem. 2014 Jan;14(1):18-28.|
|Hypoxia-mediated expression of 5-lipoxygenase-activating protein involves HIF-1alpha and NF-kappaB and microRNAs 135a and 199a-5p.|
|Gonsalves CS, Kalra VK.|
|J Immunol. 2010 Apr 1;184(7):3878-88. doi: 10.4049/jimmunol.0902594. Epub 2010 Mar 1.|
|Regulatory microRNA network identification in bovine blastocyst development.|
|Goossens K, Mestdagh P, Lefever S, Van Poucke M, Van Zeveren A, Van Soom A, Vandesompele J, Peelman L.|
|Stem Cells Dev. 2013 Jul 1;22(13):1907-20. doi: 10.1089/scd.2012.0708. Epub 2013 Mar 15.|
|Common micro-RNA signature in skeletal muscle damage and regeneration induced by Duchenne muscular dystrophy and acute ischemia.|
|Greco S, De Simone M, Colussi C, Zaccagnini G, Fasanaro P, Pescatori M, Cardani R, Perbellini R, Isaia E, Sale P, Meola G, Capogrossi MC, Gaetano C, Martelli F.|
|FASEB J. 2009 Oct;23(10):3335-46. doi: 10.1096/fj.08-128579. Epub 2009 Jun 15.|
|Tumor suppressive microRNA-1285 regulates novel molecular targets: aberrant expression and functional significance in renal cell carcinoma.|
|Hidaka H, Seki N, Yoshino H, Yamasaki T, Yamada Y, Nohata N, Fuse M, Nakagawa M, Enokida H.|
|Oncotarget. 2012 Jan;3(1):44-57.|
|miR-135a contributes to paclitaxel resistance in tumor cells both in vitro and in vivo.|
|Holleman A, Chung I, Olsen RR, Kwak B, Mizokami A, Saijo N, Parissenti A, Duan Z, Voest EE, Zetter BR.|
|Oncogene. 2011 Oct 27;30(43):4386-98. doi: 10.1038/onc.2011.148. Epub 2011 May 9.|
|miR-135a leads to cervical cancer cell transformation through regulation of beta-catenin via a SIAH1-dependent ubiquitin proteosomal pathway.|
|Leung CO, Deng W, Ye TM, Ngan HY, Tsao SW, Cheung AN, Pang RT, Yeung WS.|
|Carcinogenesis. 2014 Feb 25. [Epub ahead of print]|
|Down-regulation of some miRNAs by degrading their precursors contributes to anti-cancer effect of mistletoe lectin-I.|
|Li LN, Zhang HD, Zhi R, Yuan SJ.|
|Br J Pharmacol. 2011 Jan;162(2):349-64. doi: 10.1111/j.1476-5381.2010.01042.x.|
|A microRNA signature for a BMP2-induced osteoblast lineage commitment program.|
|Li Z, Hassan MQ, Volinia S, van Wijnen AJ, Stein JL, Croce CM, Lian JB, Stein GS.|
|Proc Natl Acad Sci U S A. 2008 Sep 16;105(37):13906-11. doi: 10.1073/pnas.0804438105. Epub 2008 Sep 10.|
|MicroRNA-135a contributes to the development of portal vein tumor thrombus by promoting metastasis in hepatocellular carcinoma.|
|Liu S, Guo W, Shi J, Li N, Yu X, Xue J, Fu X, Chu K, Lu C, Zhao J, Xie D, Wu M, Cheng S, Liu S.|
|J Hepatol. 2012 Feb;56(2):389-96. doi: 10.1016/j.jhep.2011.08.008. Epub 2011 Aug 31.|
|Genetic alterations in microRNAs in medulloblastomas.|
|Lv SQ, Kim YH, Giulio F, Shalaby T, Nobusawa S, Yang H, Zhou Z, Grotzer M, Ohgaki H.|
|Brain Pathol. 2012 Mar;22(2):230-9. doi: 10.1111/j.1750-3639.2011.00523.x. Epub 2011 Sep 15.|
|Acute stress alters amygdala microRNA miR-135a and miR-124 expression: inferences for corticosteroid dependent stress response.|
|Mannironi C, Camon J, De Vito F, Biundo A, De Stefano ME, Persiconi I, Bozzoni I, Fragapane P, Mele A, Presutti C.|
|PLoS One. 2013 Sep 4;8(9):e73385. doi: 10.1371/journal.pone.0073385. eCollection 2013.|
|Expression Profiling of microRNA in Cryptorchid Testes: miR-135a Contributes to the Maintenance of Spermatogonial Stem Cells by Regulating FoxO1.|
|Moritoki Y, Hayashi Y, Mizuno K, Kamisawa H, Nishio H, Kurokawa S, Ugawa S, Kojima Y, Kohri K.|
|J Urol. 2014 Apr;191(4):1174-80. doi: 10.1016/j.juro.2013.10.137. Epub 2013 Oct 31.|
|Regulation of the adenomatous polyposis coli gene by the miR-135 family in colorectal cancer.|
|Nagel R, le Sage C, Diosdado B, van der Waal M, Oude Vrielink JA, Bolijn A, Meijer GA, Agami R.|
|Cancer Res. 2008 Jul 15;68(14):5795-802. doi: 10.1158/0008-5472.CAN-08-0951.|
|Regulation of JAK2 by miR-135a: prognostic impact in classic Hodgkin lymphoma.|
|Navarro A, Diaz T, Martinez A, Gaya A, Pons A, Gel B, Codony C, Ferrer G, Martinez C, Montserrat E, Monzo M.|
|Blood. 2009 Oct 1;114(14):2945-51. doi: 10.1182/blood-2009-02-204842. Epub 2009 Aug 7.|
|MicroRNA expression profiling in classic Hodgkin lymphoma.|
|Navarro A, Gaya A, Martinez A, Urbano-Ispizua A, Pons A, Balague O, Gel B, Abrisqueta P, Lopez-Guillermo A, Artells R, Montserrat E, Monzo M.|
|Blood. 2008 Mar 1;111(5):2825-32. Epub 2007 Dec 18.|
|miR-135A regulates preimplantation embryo development through down-regulation of E3 Ubiquitin Ligase Seven In Absentia Homolog 1A (SIAH1A) expression.|
|Pang RT, Liu WM, Leung CO, Ye TM, Kwan PC, Lee KF, Yeung WS.|
|PLoS One. 2011;6(11):e27878. doi: 10.1371/journal.pone.0027878. Epub 2011 Nov 22.|
|MicroRNA 135 regulates HOXA10 expression in endometriosis.|
|Petracco R, Grechukhina O, Popkhadze S, Massasa E, Zhou Y, Taylor HS.|
|J Clin Endocrinol Metab. 2011 Dec;96(12):E1925-33. doi: 10.1210/jc.2011-1231. Epub 2011 Sep 28.|
|miRNAs regulate SIRT1 expression during mouse embryonic stem cell differentiation and in adult mouse tissues.|
|Saunders LR, Sharma AD, Tawney J, Nakagawa M, Okita K, Yamanaka S, Willenbring H, Verdin E.|
|Aging (Albany NY). 2010 Jul;2(7):415-31.|
|MicroRNAs miR-124 and miR-135a are potential regulators of the mineralocorticoid receptor gene (NR3C2) expression.|
|Sober S, Laan M, Annilo T.|
|Biochem Biophys Res Commun. 2010 Jan 1;391(1):727-32. doi: 10.1016/j.bbrc.2009.11.128. Epub 2009 Nov 26.|
|Stage-dependent differential expression of microRNAs in colorectal cancer: potential role as markers of metastatic disease.|
|Vickers MM, Bar J, Gorn-Hondermann I, Yarom N, Daneshmand M, Hanson JE, Addison CL, Asmis TR, Jonker DJ, Maroun J, Lorimer IA, Goss GD, Dimitroulakos J.|
|Clin Exp Metastasis. 2012 Feb;29(2):123-32. doi: 10.1007/s10585-011-9435-3. Epub 2011 Nov 26.|
|MiR-135a targets JAK2 and inhibits gastric cancer cell proliferation.|
|Wu H, Huang M, Cao P, Wang T, Shu Y, Liu P.|
|Cancer Biol Ther. 2012 Mar;13(5):281-8. doi: 10.4161/cbt.18943. Epub 2012 Mar 1.|
|MiR-135a functions as a selective killer of malignant glioma.|
|Wu S, Lin Y, Xu D, Chen J, Shu M, Zhou Y, Zhu W, Su X, Zhou Y, Qiu P, Yan G.|
|Oncogene. 2012 Aug 23;31(34):3866-74. doi: 10.1038/onc.2011.551. Epub 2011 Dec 5.|
|miR-135a/b modulate cisplatin resistance of human lung cancer cell line by targeting MCL1.|
|Zhou L, Qiu T, Xu J, Wang T, Wang J, Zhou X, Huang Z, Zhu W, Shu Y, Liu P.|
|Pathol Oncol Res. 2013 Oct;19(4):677-83. doi: 10.1007/s12253-013-9630-4. Epub 2013 May 3.|
|MiR-135a promotes growth and invasion of colorectal cancer via metastasis suppressor 1 in vitro.|
|Zhou W, Li X, Liu F, Xiao Z, He M, Shen S, Liu S.|
|Acta Biochim Biophys Sin (Shanghai). 2012 Oct;44(10):838-46.|
|This paper should be referenced as such :|
|A Navarro, M Díaz-Beyá, M Monzó_|
|MIR135A1 (microRNA 135a-1)|
|Atlas Genet Cytogenet Oncol Haematol. 2014;18(10):718-723.|
|Free journal version : [ pdf ] [ DOI ]|
|On line version : http://AtlasGeneticsOncology.org/Genes/MIR135A1ID50328ch3p21.html|
|HGNC (Hugo)||MIR135A1 31520|
|Entrez_Gene (NCBI)||MIR135A1 406925 microRNA 135a-1|
|Aliases||MIRN135-1; MIRN135A1; mir-135a-1|
|Ensembl hg19 (Hinxton)||ENSG00000207926 [Gene_View]|
|Ensembl hg38 (Hinxton)||ENSG00000207926 [Gene_View] chr3:52294219-52294308 [Contig_View] MIR135A1 [Vega]|
|Genetics Home Reference (NIH)||MIR135A1|
|Genomic and cartography|
|GoldenPath hg38 (UCSC)||MIR135A1 - chr3:52294219-52294308 - 3p21.2 [Description] (hg38-Dec_2013)|
|GoldenPath hg19 (UCSC)||MIR135A1 - 3p21.2 [Description] (hg19-Feb_2009)|
|Ensembl||MIR135A1 - 3p21.2 [CytoView hg19] MIR135A1 - 3p21.2 [CytoView hg38]|
|Mapping of homologs : NCBI||MIR135A1 [Mapview hg19] MIR135A1 [Mapview hg38]|
|Gene and transcription|
|RefSeq transcript (Entrez)|
|RefSeq genomic (Entrez)|
|Consensus coding sequences : CCDS (NCBI)||MIR135A1|
|Alternative Splicing Gallery||ENSG00000207926|
|Gene Expression||MIR135A1 [ NCBI-GEO ] MIR135A1 [ EBI - ARRAY_EXPRESS ] MIR135A1 [ SEEK ] MIR135A1 [ MEM ]|
|Gene Expression Viewer (FireBrowse)||MIR135A1 [ Firebrowse - Broad ]|
|SOURCE (Princeton)||Expression in : [Datasets]   [Normal Tissue Atlas]  [carcinoma Classsification]  [NCI60]|
|BioGPS (Tissue expression)||406925|
|GTEX Portal (Tissue expression)||MIR135A1|
|Protein : pattern, domain, 3D structure|
|Domain families : Pfam (Sanger)|
|Domain families : Pfam (NCBI)|
|Conserved Domain (NCBI)||MIR135A1|
|DMDM Disease mutations||406925|
|Human Protein Atlas||ENSG00000207926|
|Protein Interaction databases|
|Ontologies - Pathways|
|Huge Navigator||MIR135A1 [HugePedia]|
|snp3D : Map Gene to Disease||406925|
|Clinical trials, drugs, therapy|
|Chemical/Protein Interactions : CTD||406925|
|Chemical/Pharm GKB Gene||PA164722481|
|canSAR (ICR)||MIR135A1 (select the gene name)|
|PubMed||34 Pubmed reference(s) in Entrez|
|GeneRIFs||Gene References Into Functions (Entrez)|
|REVIEW articles||automatic search in PubMed|
|Last year publications||automatic search in PubMed|
Search in all EBI
|© Atlas of Genetics and Cytogenetics in Oncology and Haematology||indexed on : Mon Sep 18 17:07:59 CEST 2017|
For comments and suggestions or contributions, please contact us