TACC3 通过 ERK/Akt/cyclin D1 信号通路促进上皮间质转化促进胃癌发生。
TACC3 Promotes Gastric Carcinogenesis by Promoting Epithelial-mesenchymal Transition Through the ERK/Akt/cyclin D1 Signaling Pathway.
机构信息
Department of Pathology, Chonnam National University Research Institute of Medical Science, Chonnam National University Medical School and Hwasun Hospital, Jeollanam-do, Republic of Korea.
Department of Pharmacology and Toxicology, Sylhet Agricultural University, Sylhet, Bangladesh.
出版信息
Anticancer Res. 2021 Jul;41(7):3349-3361. doi: 10.21873/anticanres.15123.
BACKGROUND/AIM: The present study investigated the oncogenic functions of TACC3 in the progression of gastric cancer (GC).
MATERIALS AND METHODS
We analysed TACC3 in relation to cell growth, invasion capability, expression of epithelial-mesenchymal transition (EMT)-related markers, and ERK/Akt/cyclin D1 signaling factors. The correlation between the immunohistochemically confirmed expression of TACC3 and clinical factors was also analyzed.
RESULTS
The increased proliferation and invasion of TACC3-over-expressing GC cells was accompanied by altered regulation of EMT-associated markers and activation of ERK/Akt/cyclin D1 signaling. Immunohistochemical analysis of TACC3 in human GC tissues revealed that its expression is correlated with aggressive characteristics and poor prognosis of intestinal-type GC.
CONCLUSION
TACC3 contributes to gastric tumorigenesis by promoting EMT via the ERK/Akt/cyclin D1 signaling pathway. The correlation between TACC3 expression and multiple clinicopathological variables implies that its effective therapeutic targeting in GC will depend on the tumor subtype.
背景/目的：本研究旨在探讨 TACC3 在胃癌（GC）进展中的致癌功能。
材料和方法
我们分析了 TACC3 与细胞生长、侵袭能力、上皮-间充质转化（EMT）相关标志物表达以及 ERK/Akt/细胞周期蛋白 D1 信号因子之间的关系。还分析了免疫组织化学证实的 TACC3 表达与临床因素之间的相关性。
结果
过表达 TACC3 的 GC 细胞的增殖和侵袭增加伴随着 EMT 相关标志物的调节改变和 ERK/Akt/细胞周期蛋白 D1 信号通路的激活。对人 GC 组织中 TACC3 的免疫组织化学分析表明，其表达与肠型 GC 的侵袭性特征和不良预后相关。
结论
TACC3 通过 ERK/Akt/细胞周期蛋白 D1 信号通路促进 EMT 促进胃肿瘤发生。TACC3 表达与多种临床病理变量之间的相关性表明，其在 GC 中的有效治疗靶点将取决于肿瘤亚型。
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