姜黄素通过下调 E2F1 抑制 FLNA 来抑制喉鳞状细胞癌的恶性表型

Yuanchun Xie, Jingjing Qi, Ju Liu
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引用次数: 0

摘要

姜黄素是从莪术根茎中提取的一种多酚物质。由于其良好的生物活性和药理作用,已被用于抗肿瘤研究。本研究旨在探讨姜黄素对喉鳞状细胞癌(LSCC)的抗癌机制。研究采用实时定量聚合酶链反应(qRT-PCR)检测转录因子E2F1(E2F1)和丝胺A(FLNA)mRNA的表达水平。通过 Western 印迹检测 E2F1 和 FLNA 蛋白及增殖相关蛋白。细胞活力通过 MTT 法检测,流式细胞仪用于显示细胞周期分布和细胞凋亡。管形成试验用于检测细胞的血管生成能力。Transwell 是一种观察细胞迁移和侵袭的方法。在线网站JASPAR预测了E2F1与FLNA启动子的结合位点,染色质免疫沉淀(ChIP)和双荧光素酶报告实验验证了这一结合。姜黄素治疗使LSCC细胞活力降低、细胞周期延缓、血管生成减少、转移抑制和凋亡增加。姜黄素处理可以下调E2F1的表达,而E2F1的过表达会逆转姜黄素处理对LSCC细胞的影响。此外,E2F1能与FLAN启动子结合,促进FLNA的表达。与正常组织和细胞相比,FLNA在LSCC组织和细胞中的表达水平更高。E2F1敲除可抑制LSCC细胞的恶性表型,而加入FLNA后可逆转恶性表型。此外,FLNA在LSCC组织和细胞中含量较高。姜黄素通过抑制E2F1来调节FLNA的表达。最后,体内实验表明,姜黄素抑制剂抑制了LSCC肿瘤的形成。姜黄素通过抑制E2F1下调FLNA的表达,从而抑制了LSCC细胞的恶性表型和血管生成,这是LSCC的一种新的调控途径。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Curcumin suppresses the malignant phenotype of laryngeal squamous cell carcinoma through downregulating E2F1 to inhibit FLNA

Curcumin suppresses the malignant phenotype of laryngeal squamous cell carcinoma through downregulating E2F1 to inhibit FLNA

Curcumin is a kind of polyphenol substance extracted from the rhizome of Curcuma longa. Because of its good biological activity and pharmacological effects, it has been used in anti-tumor research. The aim of this study was to investigate the anti-cancer mechanism of curcumin on laryngeal squamous cell carcinoma (LSCC). Quantitative real-time polymerase chain reaction (qRT-PCR) was performed to check the expression level of transcription factor E2F1 (E2F1) and filamin A (FLNA) mRNA. E2F1 and FLNA protein and proliferation-associated protein were detected through western blot. Cell viability was showed by MTT assay, and flow cytometry was used to exhibit cell cycle distribution and cell apoptosis. Tube formation assay was used to detect the angiogenesis ability of cells. Transwell was used as a method to observe cell migration and invasion. The online website JASPAR predicted the binding site of E2F1 and FLNA promoter, and chromatin immunoprecipitation (ChIP) and dual-luciferase report experiment verified the combination. Curcumin treatment made LSCC cells viability reduce, cell cycle retardant, angiogenesis decrease, metastasis inhibition and apoptosis increase. And curcumin treatment could downregulate the expression of E2F1, and E2F1 overexpression would reverse the influence of curcumin treatment in LSCC cells. Moreover, E2F1 could bind to FLAN promoter and promote FLNA expression. The expression level of FLNA was higher in LSCC tissue and cells compared with normal tissue and cells. E2F1 knockdown inhibited malignant phenotype of LSCC cells, which would be reversed by FLNA addition. In addition, FLNA had high level in LSCC tissue and cells. Curcumin regulated FLNA expression via inhibiting E2F1. Finally, in vivo assay showed that curcumin inhibition restrained LSCC tumor formation. Curcumin downregulated FLNA expression through inhibiting E2F1, thereby suppressing the malignant phenotype and angiogenesis of LSCC cells, which was a new regulatory pathway in LSCC.

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