MiR-135b-5p promotes cetuximab resistance in colorectal cancer by regulating FOXN3

被引:2
|
作者
Peng, Chun [1 ]
Li, Xiaoqing [1 ]
Yao, Yuhui [1 ]
Nie, Yu [1 ]
Fan, Lingyao [1 ]
Zhu, Chuandong [1 ]
机构
[1] Nanjing Univ Chinese Med, Hosp Nanjing 2, Dept Oncol, Zhongfu Rd 1-1, Nanjing 210003, Jiangsu, Peoples R China
关键词
Colorectal cancer; cetuximab; miR-135b-5p; FOXN3; tumor resistance; EXPRESSION;
D O I
10.1080/15384047.2024.2373497
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Despite advances in targeted therapies, primary and acquired resistance make the treatment of colorectal cancer (CRC) a pressing issue to be resolved. According to reports, the development of CRC is linked to miRNA dysregulation. Multiple studies have demonstrated that miR-135b-5p has an aberrant expression level between CRC tissues and adjacent tissues. However, it is unclear whether there is a correlation between miR-135b-5p and cetuximab (CTx) resistance in CRC. Use the GEO database to measure miR-135b-5p expression in CRC. Additionally, RT-qPCR was applied to ascertain the production level of miR-135b-5p in three human CRC cells and NCM460 cells. The capacity of cells to migrate and invade was examined utilizing the wound-healing and transwell assays, while the CCK-8 assay served for evaluating cell viability, as well as colony formation assays for proliferation. The expected target protein of miR-135b-5p in CRC cell cetuximab resistance has been investigated using western blot. Suppression of miR-135b-5p could increase the CTx sensitivity of CTx-resistant CRC cells, as manifested by the attenuation of proliferation, migration, and invasion ability. Mechanistic studies revealed miR-135b-5p regulates the epithelial-to-mesenchymal transition (EMT) process and Wnt/beta-catenin signaling pathway through downgulating FOXN3. In short, knockdowning miR-135b-5p could increase FOXN3 expression in CRC cells, promote the EMT process, and simultaneously activate the Wnt/beta-catenin signaling pathway to elevate CTx resistance in CRC cells.
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页数:11
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