| Literature DB >> 33655506 |
Hongwen Li1, Weijie Liang2, Hongyu Zhang2, Yifang Shui3, Zhe Zhang1.
Abstract
Colorectal cancer (CRC) is one of the commonest human cancers and the fourth primary cause of cancer-related death. Previous studies have reported that miR-4429 develops anticancer function in follicular thyroid carcinoma and non-small cell lung cancer. However, whether miR-4429 is implicated in the CRC progression remains to be clarified. The aim of our current study was to explore the potential role of miR-4429 in CRC. According to the result of quantitative real-time polymerase chain reaction analysis, miR-4429 was expressed at a low level in CRC cells. Gain-of-function assays showed that the upregulation of miR-4429 inhibited cell proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) process in CRC, whereas miR-4429 inhibition led to the opposite results. It was uncovered from mechanism experiments that miR-4429 targeted forkhead box M1 (FOXM1) and therefore regulating SMAD family member 3 (SMAD3) expression. Rescue experiments elucidated that miR-4429 influenced cell proliferation, migration, invasion, and EMT process in CRC by targeting FOXM1 to inactivate SMAD3. In conclusion, our study revealed that miR-4429 targeted FOXM1 to decrease SMAD3 expression and thus impeding cell proliferation, migration, invasion, and EMT process of CRC cells.Entities:
Keywords: CRC; FOXM1; SMAD3; miR-4429
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Year: 2021 PMID: 33655506 DOI: 10.1002/jcp.30271
Source DB: PubMed Journal: J Cell Physiol ISSN: 0021-9541 Impact factor: 6.384