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MEX3A is upregulated in esophageal squamous cell carcinoma (ESCC) and promotes development and progression of ESCC through targeting CDK6

机译:Mex3a在食管鳞状细胞癌(ESCC)中上调并通过针对CDK6促进ESCC的开发和进展

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摘要

Esophageal squamous cell carcinoma (ESCC) is one of the most commonly diagnosed malignant tumors worldwide and identified as a serious threat to human health. The role of MEX3A in ESCC remains unclear. In this study, we found that MEX3A was upregulated in tumor tissues of ESCC and positively associated with more advanced tumor stage, higher risk of lymphatic metastasis and poor prognosis. The downregulation of MEX3A in ESCC cell lines could induce inhibition of cell proliferation, colony formation, cell migration, and the promotion of cell apoptosis, while MEX3A overexpression exhibited opposite effects. In vivo experiments also verified the inhibition of ESCC induced by MEX3A knockdown. Moreover, we identified CDK6 as a potential target of MEX3A, which was also upregulated in ESCC. Further studies demonstrated that knockdown of CDK6 showed similar effects on the development of ESCC with MEX3A. More importantly, it was illustrated that CDK6 knockdown could alleviate the promotion effects of MEX3A overexpression on ESCC. In conclusion, MEX3A was identified as a tumor promotor in the development and progression of ESCC by targeting CDK6, which may be considered as a novel prognostic indicator and therapeutic target in treatment of ESCC.
机译:食管鳞状细胞癌(ESCC)是全世界最常见的恶性肿瘤之一,并被确定为对人类健康的严重威胁。 MEX3A在ESCC中的作用尚不清楚。在这项研究中,我们发现MEX3A在ESCC的肿瘤组织中上调,与更晚期的肿瘤阶段呈正相关,淋巴结转移的风险较高,预后差。 MEX3A在ESCC细胞系中的下调可以诱导细胞增殖,菌落形成,细胞迁移和细胞凋亡促进的抑制,而MEX3A过表达表现出相反的效果。体内实验还验证了MEX3A敲低诱导的ESCC的抑制。此外,我们将CDK6鉴定为MEX3A的潜在靶标,这也是在ESCC中上调的。进一步的研究表明,CDK6的敲低表现出与MEX3A的ESCC发育的类似效果。更重要的是,说明CDK6敲低可以缓解MEX3A过表达对ESCC的促进效应。总之,通过靶向CDK6将MEX3A鉴定为ESCC的开发和进展中的肿瘤促进剂,这可能被视为治疗ESCC的新型预后指标和治疗靶标。

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