| Literature DB >> 31396355 |
Bao Chai1, Yarong Guo2, Xiangli Cui3, Jinchun Liu4, Yuhong Suo4, Zhangfeng Dou4, Ning Li5.
Abstract
Colon cancer is one of the most common malignancies worldwide, while the molecular mechanism remains largely unknown. miR-223-3p plays an important role in cancer development. Here, we found that miR-223-3p was up-regulated in 30 cases of colon cancer tissues as compared with their adjacent normal tissues. Lentivirus-mediated miR-223-3p over-expression promoted the proliferation, colony formation, migration and invasion of colon cancer cells. Inverse results were observed in miR-223-3p knockdown cells. Epithelial-mesenchymal transition (EMT) was regulated by miR-223-3p. In addition, cell apoptosis was suppressed and enhanced by miR-223-3p over-expression and knockdown, respectively. We further identified PRDM1, a tumor suppressor, was the target of miR-223-3p using microarray and luciferase assay. Our findings suggested that miR-223-3p acts as an oncogenic microRNA in colon cancer through regulating EMT and PRDM1.Entities:
Keywords: Colon cancer; EMT; PRDM1; miR-223-3p
Year: 2019 PMID: 31396355 PMCID: PMC6684915
Source DB: PubMed Journal: Am J Transl Res ISSN: 1943-8141 Impact factor: 4.060