Thyroid hormone receptor interactor 13 (TRIP13) is an ATPase that has been found to be overexpressed in many tumors. The aim of this study was to investigate the role of TRIP13 and its mechanism of action in lung cancer. The expression of TRIP13 was examined in lung cancer tissues and corresponding normal lung tissues by western blotting. TRIP13 was overexpressed or knocked down by transient transfection or siRNA interference in lung cancer cells, respectively. The expression of key proteins associated with the Wnt signaling pathway and epithelial-mesenchymal transition (EMT) was assessed. The interaction between TRIP13 and low-density lipoprotein receptor-related protein 6 (LRP6) was examined by co-immunoprecipitation and laser confocal immunofluorescence. Moreover, this study determined the proliferative and invasive ability of cells through colony formation, cell proliferation, and Matrigel invasion assays. The expression of TRIP13 was higher in lung cancer tissues than in normal lung tissues (p = 0.002), and this correlated with poor patient prognosis (p < 0.001). In addition, overexpression of TRIP13 enhanced the levels of active β-catenin and target proteins of the Wnt signaling pathways (p < 0.05). This study found that TRIP13 can co-localize and bind with LRP6. Furthermore, overexpression of TRIP13 caused the upregulation of N-cadherin, Snail, and vimentin, and the downregulation of E-cadherin (p < 0.05). The aforementioned results were reversed after knocking down the expression of TRIP13 (p < 0.05). TRIP13 is highly expressed in lung cancers, indicating poor prognosis. overexpression of TRIP13 promotes the proliferative and invasive ability of lung cancer cells via the activation of Wnt signaling pathway and EMT.

甲状腺激素受体相互作用物 13 (TRIP13) 是一种 ATP 酶，已发现在许多肿瘤中过度表达。本研究的目的是研究 TRIP13 的作用及其在肺癌中的作用机制。通过蛋白质印迹检测TRIP13在肺癌组织和相应的正常肺组织中的表达。TRIP13 分别通过瞬时转染或 siRNA 干扰在肺癌细胞中过表达或敲低。评估了与 Wnt 信号通路和上皮间质转化 (EMT) 相关的关键蛋白的表达。TRIP13 和低密度脂蛋白受体相关蛋白 6 (LRP6) 之间的相互作用通过免疫共沉淀和激光共聚焦免疫荧光检测。而且，本研究通过集落形成、细胞增殖和基质胶侵袭试验确定了细胞的增殖和侵袭能力。TRIP13在肺癌组织中的表达高于正常肺组织。p  = 0.002），这与患者预后不良相关（p  < 0.001）。此外，TRIP13 的过表达提高了活性 β-catenin 和 Wnt 信号通路靶蛋白的水平（p  < 0.05）。该研究发现 TRIP13 可以与 LRP6 共定位并结合。此外，TRIP13 的过表达导致 N-cadherin、Snail 和波形蛋白的上调，以及 E-cadherin 的下调（p  < 0.05）。敲低 TRIP13 的表达后，上述结果发生逆转（p < 0.05)。TRIP13在肺癌中高表达，提示预后不良。TRIP13的过表达通过激活Wnt信号通路和EMT促进肺癌细胞的增殖和侵袭能力。