期刊
CELL DEATH & DISEASE
卷 10, 期 -, 页码 -出版社
SPRINGERNATURE
DOI: 10.1038/s41419-019-1962-x
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资金
- Guangdong gastrointestinal disease research center [2017B020209003]
- National Natural Science Funds of China [81772964]
- Special Scientific Research Fund of Public Welfare Profession of National Health and Family Planning Commission [201502026]
The expression panel of plasma microRNA defined miR-532-3p as a valuable biomarker for colorectal adenoma (CRA). However, its expression pattern and function in colorectal cancer (CRC) have remained unclear. The present study investigated the expression levels of miR-532-3p and found that it was in situ downregulated both in CRA and CRC. Moreover, it functioned as a sensitizer for chemotherapy in CRC by inducing cell cycle arrest and early apoptosis via its activating effects on p53 and apoptotic signaling pathways. In addition, miR-532-3p was found to restrain cell growth, metastasis, and epithelial-mesenchymal transition (EMT) phenotype of CRC. A study on the mechanism behind these effects revealed that miR-532-3p directly binds to 3'UTR regions of ETS1 and TGM2, ultimately repressing the canonical Wnt/beta-catenin signaling. Further investigation showed that TGM2 was transcriptionally regulated by ETS1 and ETS1/TGM2 axis served as a vital functional target of miR-532-3p in suppressing CRC progression. To conclude, miR-532-3p mimics could act as potential candidate for molecular therapy in CRC through inactivation of the canonical Wnt/beta-catenin signaling and enhancement of chemosensitivity.
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