MiR-106a-5p promotes 5-FU resistance and the metastasis of colorectal cancer by targeting TGFβR2.

摘要: Background Colorectal cancer (CRC) is the third leading cause of cancer-related deaths. 5-Fluorouracil (5-FU)-based chemotherapy has always been first-line treatment. However, development 5-FU resistance seriously affects its curative effect. The aim this study was to elucidate molecular mechanisms through miR-106a-5p in CRC. Methods tissues were collected analyze and TGFβR2 expressions by qPCR. Functional experiments for evaluating cell survival metastasis conducted observe biological effects TGFβR2. rate calculated using an MTT assay; confirmed with a Transwell invasion assay Western blotting, which we used measure expression levels epithelial-mesenchymal transition (EMT) markers E-cadherin vimentin. combination miR-106a predicted Targetscan, construction luciferase reporter plasmid pGL3-basic. interplay between tested qPCR blotting. A Spearman rank analysis employed verify correlation expressions. Results MiR-106a-5p up-regulated down-regulated resistant CRC HT-29 cells. promoted suppressed apoptosis caspase 3 activity. Additionally, overexpression cells inhibited knockdown cells; contributed migration increasing vimentin decreasing functioned directly binding conferred chemoresistance cells, reduced survival, numbers, expression, increased activity Also, negatively regulated linear way tissues. Conclusion up-regulation contributes pathomechanism colorectal promoting via inhibiting target Our findings provide new promising ways clinical application TGFβR2-miR-106a axis cancer.