Abstract
Aberrant miR-129-5p expression is a key modulator of cancer development. But how the miRNA affects colorectal cancer (CRC) remains unclear. This study was designed to illustrate the underlying mechanism of miR-129-5p in CRC. MiR-129-5p expression at cellular level was assayed by qRT-PCR. Its role in CRC cell phenotypes was studied by cell function experiments. The binding relationship between miR-129-5p and TRIP13 was analyzed and verified by target changed to bioinformatics prediction and dual-luciferase detection. Furthermore, the functional mechanism based on miR-129-5p and TRIP13 in CRC was studied through rescue experiments. CRC cell lines presented prominently lower miR-129-5p levels than the normal colon epithelial cell line. The forced miR-129-5p level suppressed CRC cell growth. TRIP13 was proved to be a target of miR-129-5p in CRC cells, and miR-129-5p overexpression reduced TRIP13 expression. TRIP13 knockdown resulted in cell cycle arrest. Additionally, TRIP13 overexpression restored the impacts of miR-129-5p overexpression on cell malignant phenotypes and cell cycle. MiR-129-5p down-regulated TRIP13 expression, thereby restraining the malignant progression of CRC cells. The findings may offer a new target for molecular therapy of CRC.
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