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HOXA10通过激活p38/ERK信号通路增强食管癌细胞增殖并抑制细胞凋亡。

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

作者信息

Jiang Lifeng, Yang Qixian

机构信息

Department of Gastroenterology, The Affiliated Changzhou No. 2 People's Hospital of Nanjing Medical University, Changzhou, Jiangsu, 213003, China.

Clinical Laboratory of Diagnostics and Gastroenterology, The Affiliated Changzhou No. 2 People's Hospital of Nanjing Medical University, No. 68 Gehuzhonglu Road, Wujin District, Changzhou, Jiangsu, 213003, China.

出版信息

Open Med (Wars). 2022 Nov 3;17(1):1750-1759. doi: 10.1515/med-2022-0558. eCollection 2022.

DOI:10.1515/med-2022-0558
PMID:36407869
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9635270/
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.

摘要

食管癌(EC)是一种极具侵袭性的恶性肿瘤。同源盒A10(HOXA10)在多种肿瘤中高表达并发挥重要作用。然而,HOXA10在食管癌中的功能仍不清楚。在本研究中,观察到HOXA10在食管癌组织和细胞中高表达。有趣的是,CCK-8检测、流式细胞术和集落形成检测证实,HOXA10的过表达促进了食管癌细胞的增殖并抑制了细胞凋亡。更重要的是,蛋白质免疫印迹检测表明,HOXA10过表达的食管癌细胞中ERK和p38的磷酸化水平升高,这表明HOXA10的过表达激活了食管癌细胞中的p38/ERK信号通路。这些发现得出结论,HOXA10通过激活p38/ERK信号通路加重了食管癌的进展,为食管癌提供了一个潜在的治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1422/9635270/1cc90e03033a/j_med-2022-0558-fig005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1422/9635270/62dd84823f9c/j_med-2022-0558-fig001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1422/9635270/7d5acc74cba5/j_med-2022-0558-fig002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1422/9635270/b96d95668c94/j_med-2022-0558-fig003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1422/9635270/f8cecef3ec7b/j_med-2022-0558-fig004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1422/9635270/1cc90e03033a/j_med-2022-0558-fig005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1422/9635270/62dd84823f9c/j_med-2022-0558-fig001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1422/9635270/7d5acc74cba5/j_med-2022-0558-fig002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1422/9635270/b96d95668c94/j_med-2022-0558-fig003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1422/9635270/f8cecef3ec7b/j_med-2022-0558-fig004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1422/9635270/1cc90e03033a/j_med-2022-0558-fig005.jpg

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