RBM3 通过 PI3K/AKT 信号通路抑制皮肤鳞状细胞癌的细胞周期

Yan Huang, Weichao Sun, Danli Zhu, Li Liu, Jianguo Feng, Qian Yi
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摘要

背景:RBM3是一种关键的RNA结合蛋白,与细胞增殖和细胞周期调控等多种细胞过程有关。目的:我们旨在研究 RNA 结合图案蛋白 3(RBM3)在 cSCC 患者中的表达水平,并评估其对 cSCC 细胞能力的影响及其潜在调控机制:方法:通过免疫组化和免疫印迹法检测RBM3在cSCC组织和A431细胞中的表达。采用 Plenti-CMV-RBM3- Puro 超表达 RBM3。使用 MTT 和集落形成试验评估了 RBM3 对 cSCC 细胞增殖能力的影响。流式细胞仪测定细胞凋亡和细胞周期,Western印迹法评估 BAX、NF-κB、BCL2、CASPASE 3、CYCLIN B、CYCLIN E、CDK1、磷酸化(P)-CDK1、CDK2、P-CDK2、ERK、P-ERK、P-AMPK、AKT、P-AKT、MDM2 和 P53 的蛋白表达:结果:RBM3在cSCC组织和A431细胞中的表达明显下调。结果:RBM3 在 cSCC 组织和 A431 细胞中的表达明显下调,RBM3 的过表达明显抑制了 A431 细胞的增殖和集落形成能力。值得注意的是,RNA-seq结果显示,与RBM3相关的差异表达基因主要参与细胞周期、卵母细胞减数分裂和P53信号通路的调控,以及MAPK、AMPK、Hippo、mTOR、PI3K/AKT、Wnt、FoxO和NF-κB信号通路的调控。此外,我们的研究结果表明,过表达RBM3可通过调节PI3K/AKT信号通路抑制cSCC的细胞增殖并诱导细胞周期停滞:本研究为RBM3在cSCC细胞增殖和细胞周期中的抑制作用提供了新的见解,并突出了其治疗cSCC的潜力。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
RBM3 Inhibits the Cell Cycle of Cutaneous Squamous Cell Carcinoma through the PI3K/AKT Signaling Pathway.

Background: RBM3 is a key RNA-binding protein that has been implicated in various cellular processes, including cell proliferation and cell cycle regulation. However, its role in cutaneous squamous cell carcinoma (cSCC) remains poorly understood.

Aims: We aimed to investigate the expression levels of RNA-binding motif protein 3 (RBM3) in patients with cSCC and evaluate its effect on cell ability in cSCC and its underlying regulatory mechanisms.

Methods: The expression of RBM3 in cSCC tissues and A431 cells was determined via immunohistochemistry and western blotting. Plenti-CMV-RBM3- Puro was used to overexpress RBM3. The effect of RBM3 on the proliferation ability of cSCC cells was evaluated using MTT and colony formation assay. Cell apoptosis and cell cycle were determined using flow cytometry, while the protein expressions of BAX, NF-κB, BCL2, CASPASE 3, CYCLIN B, CYCLIN E, CDK1, phosphorylated (P)-CDK1, CDK2, P-CDK2, ERK, P-ERK, P-AMPK, AKT, P-AKT, MDM2, and P53 were assessed using western blotting.

Results: RBM3 expression was significantly downregulated in cSCC tissues and A431 cells. RBM3 overexpression significantly inhibited the cell proliferation and colony formation ability of A431. Notably, RNA-seq results showed that the differentially expressed genes associated with RBM3 were primarily involved in the regulation of the cell cycle, oocyte meiosis, and P53 signaling pathway, as well as the modulation of the MAPK, AMPK, Hippo, mTOR, PI3K/AKT, Wnt, FoxO, and NF-κB signaling pathways. Additionally, our findings demonstrated that overexpression of RBM3 inhibited cell proliferation and induced cell cycle arrest of cSCC through modulation of the PI3K/AKT signaling pathway.

Conclusion: This study provides novel insights into the suppressive roles of RBM3 in cell proliferation and the cell cycle in cSCC and highlights its therapeutic potential for cSCC.

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