TRIP6 regulates the proliferation, migration, invasion and apoptosis of osteosarcoma cells by activating the NF-κB signaling pathway
TRIP6 regulates the proliferation, migration, invasion and apoptosis of osteosarcoma cells by activating the NF-κB signaling pathway
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DOI：
10.3892/etm.2020.8466
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发表时间：
2020-03-01
影响因子：
2.7
通讯作者：
Jing, Juehua
中科院分区：
文献类型：
--
作者：
Liu, Wei;Cheng, Li;Jing, Juehua
甲状腺激素受体相互作用蛋白6（TRIP 6）是Lin-Isl-Mec（LIM）蛋白质的zyxin家族的成员，是主要在上皮细胞中表达的衔接蛋白。TRIP 6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，TRIP 6在骨肉瘤（Os）中的作用尚未报道。因此，本研究探讨TRIP 6在骨发生发展中的作用，以及TRIP 6作为治疗骨肿瘤靶点的可能性。结果表明，TRIP 6在骨细胞和临床组织中的表达水平明显高于正常成骨细胞和癌旁组织。此外，目前的结果表明，过表达TRIP 6显着增加增殖，迁移和侵袭，同时抑制凋亡的Os细胞。然而，沉默TRIP 6降低了Os细胞的增殖、迁移和侵袭，同时激活了Os细胞的凋亡。目前的结果表明，TRIP 6的过表达通过降低kappa B α抑制剂的蛋白表达水平和增加总的和磷酸化的P65水平来增加NF-κ B活化。目前的结果表明TRIP 6沉默降低NF-κ B活化。以上结果提示TRIP 6可能在促进骨细胞增殖、迁移和侵袭中发挥作用，同时抑制细胞凋亡。TRIP 6可能是一种新的骨肉瘤预后生物标志物和治疗靶点。
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-kappa B activation by decreasing the protein expression levels of inhibitor of kappa B alpha, and increasing total and phosphorylated P65 levels. The present results indicated that TRIP6 silencing decreased NF-kappa B 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.