HOXA10 enhances cell proliferation and suppresses apoptosis in esophageal cancer via activating p38/ERK signaling pathway.

IF 1.6
Open medicine (Warsaw, Poland) Pub Date : 2022-11-03 eCollection Date: 2022-01-01 DOI:10.1515/med-2022-0558
Lifeng Jiang, Qixian Yang
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引用次数: 1

Abstract

Esophageal cancer (EC) is an extremely aggressive malignant tumor. Homeobox A10 (HOXA10) is highly expressed and plays an important role in a variety of tumors. However, the function of HOXA10 in EC remains unclear. In this study, HOXA10 was observed to highly express in EC tissues and cells. Interestingly, the CCK-8 assay, flow cytometry, and colony formation assay confirmed that overexpression of HOXA10 promoted proliferation and suppressed cell apoptosis in EC cells. More importantly, the western blot assay indicated that the phosphorylation levels of ERK and p38 were elevated in EC cells overexpressed HOXA10, indicating that overexpression of HOXA10 activated p38/ERK signaling pathway in EC cells. These findings concluded that HOXA10 aggravated EC progression via activating p38/ERK signaling pathway, providing a potential therapeutic target for EC.

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HOXA10通过激活p38/ERK信号通路促进食管癌细胞增殖,抑制细胞凋亡。
食管癌是一种极具侵袭性的恶性肿瘤。Homeobox A10 (HOXA10)是一种高表达的基因,在多种肿瘤中发挥重要作用。然而,HOXA10在EC中的功能尚不清楚。本研究观察到HOXA10在EC组织和细胞中高表达。有趣的是,CCK-8实验、流式细胞术和集落形成实验证实,HOXA10的过表达促进了EC细胞的增殖,抑制了细胞凋亡。更重要的是,western blot检测显示,在过表达HOXA10的EC细胞中,ERK和p38的磷酸化水平升高,表明过表达HOXA10激活了EC细胞中p38/ERK信号通路。这些研究结果表明,HOXA10通过激活p38/ERK信号通路加速EC的进展,为EC提供了潜在的治疗靶点。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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