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作 者:杨静 王凯瑞 刘鑫佳 刘冬 杨光 YANG Jing;WANG Kairui;LIU Xinjia;LIU Dong;YANG Guang(Department of Oncology,Tangdu Hospital,Air Force Medical University,Xi′an 710038,China)
机构地区:[1]空军军医大学唐都医院肿瘤科,陕西西安710038
出 处:《胃肠病学和肝病学杂志》2025年第3期377-382,共6页Chinese Journal of Gastroenterology and Hepatology
基 金:陕西省自然科学基础研究计划(2023-JC-YB-782)。
摘 要:目的探究间充质酶同源盒1(mesenchyme homeobox 1,MEOX1)对结肠腺癌(colon adenocarcinoma,COAD)细胞增殖、凋亡和自噬的影响。方法GEPIA数据库用于分析MEOX1在COAD和正常组织中的差异表达;qRT-PCR用于检测COAD细胞中MEOX1 mRNA水平;CCK-8法、克隆形成实验和流式细胞术分别用于检测COAD细胞的增殖和凋亡;免疫荧光染色用于评估LC3的表达;Western blotting用于检测COAD细胞中Bcl-2、Bax、Caspase-3、LC3、Beclin1、p62和PI3K/Akt/mTOR信号通路相关蛋白的表达。结果GEPIA数据库分析显示,与正常组织相比,MEOX1在COAD组织中低表达(P<0.05)。与NC组相比,MEOX1过表达抑制LoVo和SW620细胞的增殖,并引起细胞凋亡率的明显上升(P<0.01)。与NC组相比,MEOX1组Bcl-2/Bax、Caspase-3、LC3-Ⅱ和Beclin1蛋白表达升高,p62、p-PI3K、p-Akt和p-mTOR蛋白表达降低(P<0.01)。结论MEOX1在COAD中低表达,MEOX1通过PI3K/Akt/mTOR信号通路诱导自噬和细胞凋亡,可能是治疗COAD新的生物标志物。Objective To investigate the impact of mesenchyme homeobox 1(MEOX1)on the proliferation,apoptosis and autophagy of colon adenocarcinoma(COAD)cells.Methods The GEPIA database was utilized to analyze the differential expression of MEOX1 in COAD tissues compared to normal tissues.qRT-PCR was performed to measure MEOX1 mRNA levels in COAD cell lines.Cell proliferation and apoptosis were assessed using CCK-8 assays,colony formation assays and flow cytometry,respectively.Immunofluorescence staining was conducted to evaluate LC3 expression.Western blotting was employed to examine the expression levels of Bcl-2,Bax,Caspase-3,LC3,Beclin1,p62 and proteins associated with the PI3K/Akt/mTOR signaling pathway in COAD cells.Results Analysis of the GEPIA database indicated that MEOX1 expression was significantly lower in COAD tissues compared to normal tissues(P<0.05).Overexpression of MEOX1 led to a reduction in the proliferation of LoVo and SW620 cells and a notable increase in the apoptosis rate when compared to the NC group(P<0.01).In the MEOX1 overexpression group,there was an increase in the protein levels of Bax/Bcl-2,Caspase-3,LC3-Ⅱand Beclin1,while protein levels of p62,phosphorylated PI3K,phosphorylated Akt and phosphorylated mTOR were decreased(P<0.01).Conclusion MEOX1 is downregulated in COAD and promotes autophagy and apoptosis through the PI3K/Akt/mTOR signaling pathway.Therefore,MEOX1 may serve as a potential biomarker for COAD treatment.
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