Accumulating evidence has suggested that thyroid hormone receptor interacting protein 6 (TRIP6) is a novel tumor-related regulator that is aberrantly expressed in multiple tumors and contributes to tumor progression and metastasis. Yet, little is known about the role of TRIP6 in cervical cancer. In the current study, we aimed to explore the expression, biological function, and regulatory mechanism of TRIP6 in cervical cancer. Here we showed that TRIP6 expression was markedly upregulated in cervical cancer tissues and cell lines. The knockdown of TRIP6 suppressed the proliferation, colony formation, and invasive potential of cervical cancer cells, whereas TRIP6 overexpression exhibited the opposite effect. Moreover, TRIP6 contributes to the activation of Yes-associated protein (YAP) by downregulating the level of YAP phosphorylation. Notably, TRIP6-mediated tumor promotion effect was partially reversed by YAP inhibition. In addition, TRIP6 knockdown retarded the in vivo tumor growth of cervical cancer of mouse xenograft models associated with downregulation of YAP activation in tumor tissues. Taken together, these results reveal a potential tumor promotion role of TRIP6 that facilitates the proliferation and invasion of cervical cancer through activation of YAP. Our study underlines the importance of the TRIP6/YAP axis in cervical cancer and suggests TRIP6 as a potential anticancer candidate for cervical cancer.

越来越多的证据表明，甲状腺激素受体相互作用蛋白6（TRIP6）是一种新型的肿瘤相关调节剂，在多种肿瘤中异常表达，并有助于肿瘤的发展和转移。然而，关于TRIP6在宫颈癌中的作用知之甚少。在本研究中，我们旨在探讨TRIP6在宫颈癌中的表达，生物学功能和调控机制。在这里，我们显示TRIP6表达在宫颈癌组织和细胞系中显着上调。TRIP6的抑制可抑制子宫颈癌细胞的增殖，集落形成和侵袭潜能，而TRIP6的过表达则表现出相反的作用。此外，TRIP6通过下调YAP磷酸化水平来促进Yes相关蛋白（YAP）的激活。值得注意的是 TRIP6介导的肿瘤促进作用被YAP抑制部分逆转。此外，TRIP6的抑制还阻碍了小鼠异种移植模型宫颈癌的体内肿瘤生长与肿瘤组织中YAP激活的下调有关。综上所述，这些结果揭示了TRIP6的潜在的肿瘤促进作用，其通过激活YAP促进宫颈癌的增殖和侵袭。我们的研究强调了TRIP6 / YAP轴在宫颈癌中的重要性，并建议TRIP6作为宫颈癌的潜在抗癌候选药物。