Protein tyrosine kinase 7‑knockdown inhibits oral squamous cell carcinoma cell viability, proliferation, migration and invasion via downregulating dishevelled segment polarity protein 3 expression

Abstract

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.

Loss of MTA2‐mediated downregulation of PTK7 inhibits hepatocellular carcinoma metastasis progression by modulating the FAK‐MMP7 axis

“…14,15 PTK7 is proposed to accelerate cancer progression by affecting tumor growth and invasion. 9,[16][17][18] However, the functional effectors and mechanism underlying PTK7-mediated HCC progression still remain unclear.…”

“…PTK7 expression is elevated in many types of cancers, including esophageal squamous cell carcinoma, 9,10 lung adenocarcinoma, 11 colorectal cancer, 12,13 and breast cancer 14,15 . PTK7 is proposed to accelerate cancer progression by affecting tumor growth and invasion 9,16–18 . However, the functional effectors and mechanism underlying PTK7‐mediated HCC progression still remain unclear.…”

PTK7, a Catalytically Inactive Receptor Tyrosine Kinase, Increases Oncogenic Phenotypes in Xenograft Tumors of Esophageal Squamous Cell Carcinoma KYSE-30 Cells

“…PTK7 is an important modulator of tumorigenesis in adult tissues and is upregulated in esophageal squamous cell carcinoma (ESCC) [6,7], colorectal cancer [8,9], and other cancers [10][11][12]. PTK7 specifically promotes proliferation, survival, migration, invasion, and wound healing, and decreases apoptosis in many cell types [6,10,[13][14][15][16]. However, PTK7 also acts as a tumor suppressor in some cell types, such as epithelial ovarian carcinoma and lung squamous cell carcinoma cells [17,18].…”