Department of Gastroenterology, Zhengzhou University People’s Hospital, Henan Provincial People’s Hospital, Zhengzhou, Henan 450003, China.
Clinical Medicine College, Xinxiang Medical University, Xinxiang, Henan 453000, China.
Aging (Albany NY). 2024 Aug 9;16(15):11729-11743. doi: 10.18632/aging.206059.
Colon cancer is a common malignant tumor of the gastrointestinal system, which is characterized by high morbidity and mortality. The purpose of this study was to analyze the expression and biological role of miR-181a-2-3p in colon cancer and to investigate the molecular mechanism of its regulatory effect on colon cancer through stimulator of interferon genes (STING).
Real-time reverse transcription polymerase chain reaction (qRT-PCR) assay was used to detect the expression of miR-181a-2-3p in colon cancer cell lines and normal intestinal epithelial cells. After overexpression of miR-181a-2-3p in colon cancer cell lines SW480 and HT29, cells were examined by CCK8, Transwell, and flow cytometry assays for alterations in proliferation, migration, apoptosis, and cell cycle. Target genes of miR-181a-2-3p were predicted by bioinformatics and validated by dual luciferase assays. Rescue experiments were performed to explore the role of STING in the effect of miR-181a-2-3p. The effect of miR-181a-2-3p on colon cancer proliferation was validated by nude mouse tumorigenicity assay.
miR-181a-2-3p was lowly expressed in both colon cancer tissues and cell lines. Overexpression of miR-181a-2-3p led to reduced proliferation and migration, increased apoptosis, and altered cell cycle in colon cancer cell lines SW480 and HT29. STING was a target gene of miR-181a-2-3p. Increased STING expression partially counteracted the effect of overexpression of miR-181a-2-3p on colon cancer cell lines. miR-181a-2-3p also suppressed colon cancer proliferation .
miR-181a-2-3p inhibits the proliferation and oncogenicity of colon cancer, and its molecular mechanism could be inhibited by STING.
结肠癌是一种常见的胃肠道系统恶性肿瘤，其发病率和死亡率均较高。本研究旨在分析微小 RNA-181a-2-3p（miR-181a-2-3p）在结肠癌中的表达及其对结肠癌的调控作用机制，通过干扰素基因刺激因子（STING）进行研究。
采用实时逆转录聚合酶链反应（qRT-PCR）检测结肠癌细胞系和正常肠上皮细胞中 miR-181a-2-3p 的表达。在结肠癌细胞系 SW480 和 HT29 中转染 miR-181a-2-3p 过表达载体后，通过 CCK8、Transwell 和流式细胞术检测细胞增殖、迁移、凋亡和细胞周期的变化。通过生物信息学预测 miR-181a-2-3p 的靶基因，并通过双荧光素酶报告基因验证。通过 rescue 实验探讨 STING 在 miR-181a-2-3p 作用中的作用。通过裸鼠肿瘤生成实验验证 miR-181a-2-3p 对结肠癌增殖的影响。
miR-181a-2-3p 在结肠癌组织和细胞系中均低表达。过表达 miR-181a-2-3p 可导致结肠癌细胞系 SW480 和 HT29 的增殖和迁移减少，凋亡增加，细胞周期改变。STING 是 miR-181a-2-3p 的靶基因。增加 STING 表达可部分逆转 miR-181a-2-3p 过表达对结肠癌细胞系的作用。miR-181a-2-3p 还抑制结肠癌的增殖。
miR-181a-2-3p 抑制结肠癌的增殖和致癌性，其分子机制可能是通过 STING 抑制。
