Liu Wei, Cheng Li, Li Qingning, Jing Juehua
Department of Orthopedics, The Second Affiliated Hospital of Anhui Medical University, Hefei, Anhui 230601, P.R. China.
Exp Ther Med. 2020 Mar;19(3):2317-2325. doi: 10.3892/etm.2020.8466. Epub 2020 Jan 22.
Thyroid hormone receptor-interacting protein 6 (TRIP6), a member of the zyxin family of Lin-Isl-Mec (LIM) proteins, is an adaptor protein primarily expressed in epithelial cells. TRIP6 can regulate a variety of cellular responses, such as actin cytoskeletal reorganization and cell adhesion. However, to the best of our knowledge, the role of TRIP6 in osteosarcoma (Os) has not been previously reported. Therefore, the present study investigated the role of TRIP6 in the occurrence and development of Os, and the potential of utilizing TRIP6 as a therapeutic target in Os. The present results suggested that the expression levels of TRIP6 were significantly increased in Os cells and clinical tissue specimens compared with normal osteoblasts and adjacent non-tumor tissue. Moreover, the present results suggested that overexpressing TRIP6 significantly increased proliferation, migration and invasion, while inhibiting apoptosis in Os cells. However, silencing TRIP6 decreased proliferation, migration and invasion, while activating apoptosis in Os cells. The present results suggested that overexpression of TRIP6 increased NF-κB activation by decreasing the protein expression levels of inhibitor of κBα, and increasing total and phosphorylated P65 levels. The present results indicated that TRIP6 silencing decreased NF-κB activation. Collectively, the present results suggested that TRIP6 may play a role in promoting Os cell proliferation, migration and invasion, while inhibiting cell apoptosis. Furthermore, TRIP6 may be utilized as a novel prognostic biomarker and therapeutic target in Os.
甲状腺激素受体相互作用蛋白6（TRIP6）是Lin-Isl-Mec（LIM）蛋白家族中zyxin家族的成员，是一种主要在上皮细胞中表达的衔接蛋白。TRIP6可以调节多种细胞反应，如肌动蛋白细胞骨架重组和细胞粘附。然而，据我们所知，TRIP6在骨肉瘤（Os）中的作用此前尚未见报道。因此，本研究探讨了TRIP6在Os发生发展中的作用，以及将TRIP6用作Os治疗靶点的潜力。目前的结果表明，与正常成骨细胞和相邻非肿瘤组织相比，Os细胞和临床组织标本中TRIP6的表达水平显著升高。此外，目前的结果表明，过表达TRIP6显著增加了Os细胞的增殖、迁移和侵袭，同时抑制了细胞凋亡。然而，沉默TRIP6则降低了Os细胞的增殖、迁移和侵袭，同时激活了细胞凋亡。目前的结果表明，TRIP6的过表达通过降低κBα抑制剂的蛋白表达水平，以及增加总P65和磷酸化P65水平，从而增加了NF-κB的激活。目前的结果表明，沉默TRIP6可降低NF-κB的激活。总的来说，目前的结果表明，TRIP6可能在促进Os细胞增殖、迁移和侵袭，同时抑制细胞凋亡方面发挥作用。此外，TRIP6可能作为Os的一种新型预后生物标志物和治疗靶点。
