Jin Xiaoye, Huang Tao, Ma Caihong, Duan Jiafeng, Li Rong, Zhang Wei, Tian Wenyan
Department of Stomatology, The Second Hospital of Yulin City, Xi'an Jiaotong University Medical School, Yulin, Shaanxi 719000, P.R. China.
Disinfection Supply Center, The Second Hospital of Yulin City, Xi'an Jiaotong University Medical School, Yulin, Shaanxi 719000, P.R. China.
Exp Ther Med. 2021 Dec;22(6):1372. doi: 10.3892/etm.2021.10806. Epub 2021 Sep 28.
Protein tyrosine kinase 7 (PTK7) expression has been reported to be dysregulated and to regulate various cellular activities in numerous types of cancer. However, to the best of our knowledge, the status and role of PTK7 in oral squamous cell carcinoma (OSCC) remains largely unknown. The present study aimed to investigate the involvement of PTK7 in OSCC progression and to determine the potential underlying mechanisms of action. The expression levels of PTK7 and dishevelled segment polarity protein 3 (DVL3) in OSCC cell lines were analyzed using reverse transcription-quantitative PCR and western blotting. A co-immunoprecipitation assay was used to verify the binding association between PTK7 and DVL3. In addition, OSCC cells were transfected with a short hairpin RNA targeting PTK7 or pcDNA-DVL3 overexpression vectors. The effect of PTK7 on OSCC cell viability, proliferation, migration and invasion, and the underlying mechanisms, were investigated using Cell Counting Kit-8, colony formation, wound healing and Transwell assays, respectively. Western blotting was used to analyze the expression levels of proliferation- and migration-associated proteins. The results revealed that the expression levels of both PTK7 and DVL3 were significantly upregulated in OSCC cell lines. In addition, a binding association was identified between PTK7 and DVL3 in SCC-9 cells. The knockdown of PTK7 expression inhibited OSCC cell viability, proliferation, invasion and migration, while the overexpression of DVL3 reversed the inhibitory effects of PTK7-knockdown on OSCC cells. In conclusion, the results of the present study suggested that PTK7 may be a key regulator of OSCC proliferation, migration and invasion, and PTK7-knockdown may inhibit OSCC cell viability, proliferation, invasion and migration by downregulating DVL3 expression. Therefore, PTK7 and DVL3 may represent potential biomarkers for diagnosis and treatment, as well as promising drug targets for OSCC.
据报道，蛋白酪氨酸激酶7（PTK7）表达失调，并在多种类型癌症中调节各种细胞活动。然而，据我们所知，PTK7在口腔鳞状细胞癌（OSCC）中的状态和作用仍 largely未知。本研究旨在探讨PTK7在OSCC进展中的作用，并确定其潜在的作用机制。采用逆转录定量PCR和蛋白质印迹法分析OSCC细胞系中PTK7和散乱段极性蛋白3（DVL3）的表达水平。采用免疫共沉淀试验验证PTK7与DVL3之间的结合关系。此外，用靶向PTK7的短发夹RNA或pcDNA-DVL3过表达载体转染OSCC细胞。分别采用细胞计数试剂盒-8、集落形成、伤口愈合和Transwell试验研究PTK7对OSCC细胞活力、增殖、迁移和侵袭的影响及其潜在机制。采用蛋白质印迹法分析增殖和迁移相关蛋白的表达水平。结果显示，PTK7和DVL3在OSCC细胞系中的表达水平均显著上调。此外，在SCC-9细胞中鉴定出PTK7与DVL3之间的结合关系。PTK7表达的敲低抑制了OSCC细胞的活力、增殖、侵袭和迁移，而DVL3的过表达逆转了PTK7敲低对OSCC细胞的抑制作用。总之，本研究结果表明，PTK7可能是OSCC增殖、迁移和侵袭的关键调节因子，PTK7敲低可能通过下调DVL3表达抑制OSCC细胞活力、增殖、侵袭和迁移。因此，PTK7和DVL3可能是诊断和治疗的潜在生物标志物，也是OSCC有前景的药物靶点。
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