MiR-5195-3p predicts clinical prognosis and represses colorectal cancer progression by targeting TLR4/MyD88 signaling

被引:0
作者
Lv, Yandong [1 ]
Guo, Shuwei [1 ]
Jin, Lingtong [1 ]
Wang, Kai [1 ]
Li, Yongsheng [1 ]
Li, Haonan [1 ]
Lu, Yikang [1 ]
Liu, Hongzhou [1 ]
机构
[1] Changzhi Med Coll, Heping Hosp, Dept Colorectal Surg, 110 Yanan South Rd, Changzhi 046000, Shanxi, Peoples R China
关键词
miR-5195-3p; Prognosis; Colorectal cancer; TLR4; MyD88; TOLL-LIKE RECEPTORS; INFLAMMATORY MICROENVIRONMENT; CELL-PROLIFERATION; CONTRIBUTES; ACTIVATION; EXPRESSION; MICRORNAS; CARCINOMA; MIGRATION; TLR4;
D O I
10.1186/s13008-024-00133-x
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
BackgroundRecent studies have highlighted the role of miR-5195-3p in suppressing cell growth in various cancers. However, the specific functional impact of miR-5195-3p in colorectal cancer (CRC) remain to be fully clarified. The importance of miR-5195-3p in CRC was evaluated, aiming to uncover its underlying molecular mechanism and identify it as a potential therapeutic target for CRC.ResultsOur research has shown that miR-5195-3p is markedly under-expressed in CRC tissues and cell cultures, with its reduced presence associated with a higher TNM stage, lymphatic invasion, and unfavorable survival outcome. Ectopic miR-5195-3p expression curtailed proliferation, migration, and invasion of SW1116 and HT29 cells. Additionally, we discovered that miR-5195-3p directly targets and negatively influences Toll-like receptor 4 (TLR4) in CRC cells. Moreover, an inverse relationship was noted between miR-5195-3p and TLR4 expression in CRC tissue samples. Notably, restoring TLR4 expression counteracted miR-5195-3p's suppressive impact on cell growth, motility, invasiveness, epithelial-mesenchymal transition (EMT), and the TLR4/MyD88 signaling pathway in SW1116 and HT29 cells.ConclusionsMiR-5195-3p suppresses the CRC cellular functions through the downregulation of TLR4/MyD88 signaling, indicating that targeting miR-5195-3p might offer a viable therapeutic strategy for CRC.
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页数:10
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