Unknown,Transcriptomics,Genomics,Proteomics

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Repression of OSMR and FGFR1 by miR-1/133a prevents adult cardiomyocyte dedifferentiation and cell cycle entry in the adult heart

ABSTRACT: Deletion of the miR-1/133a clusters in adult cardiomyocytes results in upregulation of miRNA target genes FGFR1 and OSMR. Additional deletion of these miRNA target genes reveals a co-operative role of these receptors in the control of the cardiomyocyte differentiation state and in repression of cardiomyocyte cell cycle re-entry.

ORGANISM(S): Mus musculus

SUBMITTER: Thomas Boettger

PROVIDER: E-MTAB-10226 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Project description:For many oncogenes, increased expression resulting from copy number gain confers a selective advantage to cells that consequently make up the tumour bulk. To identify oncogenes of potential biological significance in cervical squamous cell carcinoma (SCC), 36 primary samples and ten cell lines were screened by array comparative genomic hybridization (CGH). The most commonly occurring regions of copy number gain that also showed amplification were 5p15.2–14.3 (59%), 5p13.3 (65%), and 5p13.2–13.1 (63%). Gene copy numbers were significantly associated with expression levels for three candidate oncogenes at these loci: OSMR (oncostatin M receptor) (p = 0.03), PDZK3 (PDZ domain containing protein 3) (p = 0.04), and TRIO (triple functional domain) (p = 0.03). Further examination by fluorescence in situ hybridization on a tissue microarray of 110 primary cervical SCC samples revealed copy number gain frequencies of 60.9%, 57.3%, and 54.5% for OSMR, PDZK3, and TRIO, respectively, with OSMR adversely influencing overall patient survival independently of tumour stage (p = 0.046). By array CGH, copy number gain of OSMR was not seen in any of 40 microdissected precursor cervical squamous intraepithelial lesions (SILs). Moreover, global mRNA expression analysis, using Affymetrix U133A 2.0 Arrays, showed no overexpression of OSMR in SILs, suggesting that OSMR gain and overexpression are relatively late steps in cervical carcinogenesis. In the cervical SCC cell lines CaSki and SW756, exogenous OSM activated downstream-signalling elements of OSMR including STAT3, p44/42 MAPK, and S6 ribosomal protein, and induced transcription of the angiogenic factor VEGF, effects that were reduced by OSMR depletion using RNA interference. We conclude that copy number gain of OSMR is frequently found in cervical SCC and is associated with adverse clinical outcome. As well as being a potential prognostic marker, OSMR is a candidate cell surface therapeutic target aCGH of high grade late stage primary cervical SCCs obtained from the archives of the Kidwai Memorial Institute of Oncology,

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Repression of OSMR and FGFR1 by miR-1/133a prevents adult cardiomyocyte dedifferentiation and cell cycle entry in the adult heart

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