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

• Published in: International journal of molecular sciences Vol. 23; no. 4; p. 2391
• Main Authors: Shin, Won-Sik, Park, Mi-Kyung, Kim, Jae Hoon, Oh, Si Won, Jang, Ji-Yun, Lee, Ho, Lee, Seung-Taek
• Format: Journal Article
• Language: English
• Published: Switzerland MDPI AG 21-02-2022; MDPI
• Subjects: Adhesion; AKT protein; Apoptosis; Cell cycle; Cell growth; Cell proliferation; Epigenetics; Esophageal cancer; esophageal squamous cell carcinoma; Esophagus; Extracellular signal-regulated kinase; Genes; Growth factors; Kinases; KYSE-30 cells; Molecular weight; Mutation; oncogene; Phenotypes; Phosphorylation; Protein-tyrosine kinase receptors; Proteins; PTK7; receptor protein tyrosine kinase; Squamous cell carcinoma; Therapeutic targets; Tumor cell lines; Tumorigenesis; Tumors; Tyrosine; Wound healing; Xenografts; Xenotransplantation; KYSE-30 cells; esophageal squamous cell carcinoma; oncogene; receptor protein tyrosine kinase; PTK7
• ISSN: 1422-0067; 1661-6596; 1422-0067
• DOI: 10.3390/ijms23042391

Protein tyrosine kinase 7 (PTK7), a catalytically defective receptor protein tyrosine kinase, is upregulated in tumor tissues and cell lines of esophageal squamous cell carcinoma (ESCC). We showed that PTK7 plays an oncogenic role in various ESCC cell lines. However, its role as an oncogene has not been demonstrated in vivo. Here, we examined the influence of PTK7 on the tumorigenic potential of ESCC KYSE-30 cells, which are known to establish xenograft tumors. Overexpression of PTK7 enhanced the proliferation, adhesion, wound healing, and migration of KYSE-30 cells, and these effects were reversed by the knockdown of
.
overexpression and knockdown, respectively, increased and decreased the tyrosine phosphorylation of cellular proteins and the phosphorylation of ERK, AKT, and FAK, which are important for cell proliferation, survival, adhesion, and migration. Additionally,
overexpression and silencing, respectively, increased and decreased the weight, volume, and number of Ki-67-positive proliferating cells in xenograft tumors of KYSE-30 cells. Therefore, we propose that PTK7 plays an important role in the tumorigenesis of ESCC cells in vivo and is a potential therapeutic target for ESCC.