miR-143 Inhibits Cell Proliferation of Gastric Cancer Cells Through Targeting GATA6
| Autor: | Liu Ran, Qin Yanru, Mao Guoping |
|---|---|
| Rok vydání: | 2018 |
| Předmět: |
0301 basic medicine
Cancer Research Apoptosis GATA-binding factor 6 (GATA6) Article 03 medical and health sciences 0302 clinical medicine Downregulation and upregulation Stomach Neoplasms GATA6 Transcription Factor microRNA Biomarkers Tumor Tumor Cells Cultured Humans Neoplasm Invasiveness Gastric cancer (GC) Cell proliferation Regulation of gene expression Cell growth Chemistry Cell Cycle General Medicine Cell cycle Prognosis miR-143 Gene Expression Regulation Neoplastic MicroRNAs 030104 developmental biology Oncology Cell culture 030220 oncology & carcinogenesis Cancer cell Cancer research |
| Zdroj: | Oncology Research |
| ISSN: | 1555-3906 |
| Popis: | Recent studies have suggested that the dysregulation of microRNAs (miRNAs) plays a critical role in the progression of human cancers, including gastric cancer (GC). miR-143 had been reported to function as a tumor suppressor in GC. However, the exact molecular mechanism of how miR-143 participates in GC progression remains to be determined. In this present study, we revealed that the expression of miR-143 was significantly downregulated in human GC tissues and cell lines compared with normal tissues and a normal gastric epithelium cell line. In addition, upregulation of the expression of miR-143 in a GC cell line inhibited cell proliferation and induced cell cycle arrested in the G0/G1 phase. Furthermore, GATA6 was identified as a direct target of miR-143 in GC using the luciferase reporter assay. Upregulation of miR-143 inhibited the expression of GATA6 in GC cell lines. Moreover, the overexpression of GATA6 could attenuate the effect of miR-143 on cell proliferation in the GC cell lines. Collectively, these data indicated that miR-143 plays a tumor suppressor role partly through regulating the expression of GATA6 in GC. Therefore, targeting miR-143 may be a novel therapeutic method for GC. |
| Databáze: | OpenAIRE |
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