MiR-629-5p promotes colorectal cancer progression through targetting CXXC finger protein 4

Abstract

MiR-629-5p has been shown to function as a tumor promoter in some types of cancer. However, the role of miR-629-5p in colorectal cancer remains unclear. Here, the significant up-regulation of miR-629-5p in colorectal cancer tissues and cell lines was observed. Overexpression of miR-629-5p showed a positive effect on cell proliferation and migration. The enhanced miR-629-5p level also suppressed cell apoptosis and resulted in a low Bax level and a high Bcl-2 level. Further down-regulating miR-629-5p demonstrated opposite effects. CXXC finger protein 4 (CXXC4) was predicted as a direct target of miR-629-5p. Dual-luciferase reporter and Western blotting assays exhibited miR-629-5p directly bound to the 3′UTR of CXXC4 and then down-regulated its expression at post-transcriptional level. CXXC4 knockdown rescued the decreased cell proliferation and migration and the enhanced cell apoptosis induced by inhibiting miR-629-5p expression. Notably, overexpression of miR-629-5p also conferred 5-fluorouracil sensitivity, which was partly abrogated by coexpression of CXXC4. Overall, the results presented here suggest that miR-629-5p functions as a tumor promoter by improving proliferation and migration and repressing apoptosis and 5-FU sensitivity in colorectal cancer progression by directly down-regulating CXXC4.

GC-Derived EVs Enriched with MicroRNA-675-3p Contribute to the MAPK/PD-L1-Mediated Tumor Immune Escape by Targeting CXXC4

“… 28 The evidence derived from our study suggested that miR-675-3p targeted CXXC4. A previous study suggested that miR-629 is able to accelerate the progression of cancer by binding to CXXC4 in colorectal cancer cells, 29 which further validates our findings that CXXC4 could be a target gene of miRNA. We also evaluated the relationship between miR-675-3p and PD-L1, which showed that GC-EV-delivered miR-675-3p not only promoted PD-L1 expression, but it also suppressed the activation of T cells in GC modeled mice.…”

Upregulation of Serum miR-629 Predicts Poor Prognosis for Non-Small-Cell Lung Cancer

“…In addition, an in vitro assay showed that overexpression of miR-629 promoted the proliferation, migration, and invasiveness of HCC cells, while knockdown of miR-629 led to the opposite effects [18]. In colorectal cancer, miR-629 was found to be significantly upregulated in colorectal cancer tissues and cell lines, and upregulation of miR-629 enhanced cell proliferation and migration as well as suppressed cell apoptosis by directly downregulating CXXC4 [19].…”

Paeoniflorin attenuates DHEA-induced polycystic ovary syndrome via inactivation of TGF-β1/Smads signaling pathway in vivo

“…MI is a second messenger of follicle-stimulating hormone (FSH) and DCI is an aromatase inhibitor in the human ovary [ 35 ]. Previous research found that PAE significantly decreased serum insulin and glucagon levels, improved insulin sensitivity and serum lipids profiles, and alleviated hepatic steatosis in Sprague-Dawley rats [ 36 ]. Therefore, we speculated that one of the possible mechanisms by which PAE improved ovarian fibrosis should be related to the reduction in androgen levels and inhibition of TGF-β1/Smads signaling pathway by improving insulin resistance.…”