Department of Infectious Diseases, Renmin Hospital, Hubei University of Medicine, Shiyan, Hubei 442000, P.R. China.
Mol Med Rep. 2021 Feb;23(2). doi: 10.3892/mmr.2020.11793. Epub 2020 Dec 23.
The tumour suppressor gene F‑box and WD repeat domain‑containing 7 () plays an important role in human cancer by regulating cell division, proliferation and differentiation. However, the exact regulatory mechanisms of microRNA (miR)‑223 in colorectal cancer (CRC) cells are still unknown. The present study aimed to investigate the effect and mechanism of miR‑223 inhibiting on the proliferation and apoptosis of CRC cells. HCT116 cells were transfected with miR‑223 mimics or small interfering RNA (siRNA) targeting (si), and the effects of these treatments on cell proliferation and apoptosis were examined. The downstream Notch and Akt/mTOR pathways were also assessed. Following miR‑223 overexpression, the mRNA and protein expression levels of FBXW7 were downregulated. Transfection with miR‑223 mimics or si promoted the proliferation of HCT116 cells and inhibited apoptosis by promoting the Notch and Akt/mTOR signalling pathways. Conversely, miR‑223 mimics transfection with FBXW7 overexpression inhibited cell viability and restored apoptosis. Thus, the present study demonstrated that miR‑223 could bind to the gene and inhibit its expression, ultimately increasing the proliferation and preventing the apoptosis of CRC cells through the Notch and Akt/mTOR signalling pathways.
抑癌基因 F‑box 和 WD 重复域蛋白 7() 通过调节细胞分裂、增殖和分化在人类癌症中发挥重要作用。然而,miR-223 在结直肠癌(CRC)细胞中的确切调节机制仍不清楚。本研究旨在探讨 miR-223 抑制对 CRC 细胞增殖和凋亡的影响及其机制。将 miR-223 模拟物或靶向()的小干扰 RNA(si)转染至 HCT116 细胞,检测这些处理对细胞增殖和凋亡的影响。还评估了下游 Notch 和 Akt/mTOR 通路。miR-223 过表达后,FBXW7 的 mRNA 和蛋白表达水平下调。转染 miR-223 模拟物或 si 促进 HCT116 细胞的增殖,并通过促进 Notch 和 Akt/mTOR 信号通路抑制细胞凋亡。相反,转染 FBXW7 过表达 miR-223 模拟物抑制细胞活力并恢复细胞凋亡。因此,本研究表明,miR-223 可以与基因结合并抑制其表达,最终通过 Notch 和 Akt/mTOR 信号通路增加 CRC 细胞的增殖并防止其凋亡。