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补体C1s在食管鳞状细胞癌中的表达及生物学作用

The expression and biological role of complement C1s in esophageal squamous cell carcinoma.

作者信息

Ge Ruomu, Luan Zhengyun, Guo Ting, Xia Sheng, Ye Jun, Xu Jie

机构信息

Anhui Province Key Laboratory of Infectious Diseases, The First Affiliated Hospital of Anhui Medical University, Hefei, China.

Central Laboratory, The Affiliated Taizhou People's Hospital of Nanjing Medical University, Taizhou School of Clinical Medicine, Nanjing Medical University, Taizhou, Jiangsu, 225300, P.R. China.

出版信息

Open Life Sci. 2024 Jul 24;19(1):20220915. doi: 10.1515/biol-2022-0915. eCollection 2024.

Abstract

The present work focused on investigating the role of the altered expression of complement C1s in proliferation and apoptosis of esophageal squamous cell carcinoma (ESCC) cells and explore its biological functions in ESCC, so as to lay a theoretical foundation and provide certain clinical reference for diagnosing and treating ESCC. Complement C1s expression within ESCC was assessed, and its clinical pathological characteristics in ESCC patients were analyzed. Subsequently, experiments were performed to further explore the mechanisms by which complement C1s affected ESCC. According to the results, complement C1s expression within ESCC markedly increased relative to adjacent non-cancerous samples. High C1s expression showed positive relation to race, residual lesion, and tumor location of ESCC patients. Complement C1s affected ESCC cell proliferation and apoptosis. Notably, C1s knockdown significantly inhibited ESCC cell proliferation and enhanced their apoptosis. C1s suppressed ESCC cell proliferation via Wnt1/β-catenin pathway and promoted their apoptosis through modulating the expression of Bcl2, Bax, and cleaved-caspase3.

摘要

本研究聚焦于探讨补体C1s表达改变在食管鳞状细胞癌(ESCC)细胞增殖和凋亡中的作用,并探究其在ESCC中的生物学功能,从而为ESCC的诊断和治疗奠定理论基础并提供一定的临床参考。评估了ESCC中补体C1s的表达,并分析了其在ESCC患者中的临床病理特征。随后,进行实验以进一步探究补体C1s影响ESCC的机制。结果显示,与相邻非癌组织样本相比,ESCC中补体C1s的表达显著增加。高C1s表达与ESCC患者的种族、残留病灶及肿瘤位置呈正相关。补体C1s影响ESCC细胞的增殖和凋亡。值得注意的是,敲低C1s可显著抑制ESCC细胞增殖并增强其凋亡。C1s通过Wnt1/β-连环蛋白途径抑制ESCC细胞增殖,并通过调节Bcl2、Bax和裂解型半胱天冬酶-3的表达促进其凋亡。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c9f/11282917/21a0724fff78/j_biol-2022-0915-fig001.jpg

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