Loss of RBMS1 as a regulatory target of miR-106b influences cell growth, gap closing and colony forming in prostate carcinoma
| Autor: | Sven Wach, Jaroslaw Thomas Dankert, Gunther Wennemuth, Elena Dilâra Czyrnik, Marc Wiesehöfer |
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| Jazyk: | angličtina |
| Rok vydání: | 2020 |
| Předmět: |
Male
0301 basic medicine Medizin lcsh:Medicine Apoptosis Biology Article 03 medical and health sciences Prostate cancer 0302 clinical medicine Downregulation and upregulation DU145 Cell Movement Prostate microRNA LNCaP Gene expression Cancer genomics Biomarkers Tumor Tumor Cells Cultured medicine Humans ddc:610 lcsh:Science Tumor Stem Cell Assay Cell Proliferation Multidisciplinary lcsh:R Cell Cycle Prostatic Neoplasms RNA-Binding Proteins Cancer Prognosis medicine.disease DNA-Binding Proteins Gene Expression Regulation Neoplastic MicroRNAs 030104 developmental biology medicine.anatomical_structure 030220 oncology & carcinogenesis Cancer research lcsh:Q |
| Zdroj: | Scientific Reports Scientific Reports, Vol 10, Iss 1, Pp 1-12 (2020) |
| Popis: | Prostate carcinoma (PCa) is the second most commonly diagnosed cancer in males worldwide. Among hereditary genetic mutations and nutrient factors, a link between the deregulation of microRNA (miRNA) expression and the development of prostate carcinoma is assumed. MiRNAs are small non-coding RNAs which post-transcriptionally regulate gene expression and which are involved in tumour development and progression as oncogenes or tumour suppressors. Although many genes could be confirmed as targets for deregulated miRNAs, the impact of differentially expressed miRNA and their regulatory target genes on prostate tumour development and progression are not fully understood yet. We could validate RBMS1, a barely described RNA-binding protein, as a new target gene for oncogenic miR-106b, which was identified as an induced miRNA in PCa. Further analysis revealed a loss of RBMS1 expression in prostate tumours compared to corresponding normal tissue. Overexpression of RBMS1 in DU145 and LNCaP prostate cancer cells resulted in diminished cell proliferation, colony forming ability as well as in retarded gap closing. Our results demonstrate for the first time a miR-106b dependent downregulation of RBMS1 in prostate carcinoma. Additionally, we show new tumour suppressive properties of RBMS1 whose observed loss may further elucidate the development of PCa. |
| Databáze: | OpenAIRE |
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