FAIM-S 作为 NF-κB 通路的负调控因子，阻止 NSCLC 细胞的细胞周期进程。
FAIM-S functions as a negative regulator of NF-κB pathway and blocks cell cycle progression in NSCLC cells.
机构信息
Department of Burn, The First Affiliated Hospital of Nanchang University , Nanchang, P.R.China.
Jiangxi Institute of Respiratory Disease, The First Affiliated Hospital of Nanchang University , Nanchang, P.R.China.
出版信息
Cell Cycle. 2020 Dec;19(24):3458-3467. doi: 10.1080/15384101.2020.1843811. Epub 2020 Nov 29.
Tumorigenesis is closely related to the disorder of the cell cycle. The cell cycle progression includes the interphase (G0/G1, S, and G2 phase) and mitosis (M phase). CCND1 is a key protein that regulates the entry of the G0/G1 phase into the S phase. In our study, we found that the short form of Fas Apoptosis Inhibitory Molecule 1 (FAIM-S) could regulate the expression of CCND1 and had a tumor-suppressing role in non-small cell lung cancer (NSCLC). Overexpressing FAIM-S significantly inhibited the proliferation and cell cycle progression in NSCLC cells. Further studies demonstrated that FAIM-S could interact with IKK-α, reducing its protein stability. This effect led to the suppression of the NF-κB pathway, resulting in the decreased expression of CCND1. Thus, our study demonstrated that FAIM-S functioned as a negative regulator of the NF-κB pathway and played a tumor-suppressing role through blocking cell cycle progression in NSCLC cells.
肿瘤发生与细胞周期紊乱密切相关。细胞周期进程包括间期（G0/G1、S 和 G2 期）和有丝分裂（M 期）。CCND1 是一种关键蛋白，可调节 G0/G1 期进入 S 期。在我们的研究中，我们发现 Fas 凋亡抑制分子 1（FAIM-S）的短形式可以调节 CCND1 的表达，并在非小细胞肺癌（NSCLC）中具有肿瘤抑制作用。过表达 FAIM-S 可显著抑制 NSCLC 细胞的增殖和细胞周期进程。进一步的研究表明，FAIM-S 可以与 IKK-α 相互作用，降低其蛋白质稳定性。这种作用抑制了 NF-κB 通路，导致 CCND1 的表达减少。因此，我们的研究表明，FAIM-S 作为 NF-κB 通路的负调节剂发挥作用，通过阻断 NSCLC 细胞的细胞周期进程发挥肿瘤抑制作用。
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