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Updated: Feb 9, 2026
Development of Compendium for Esophageal Squamous Cell Carcinoma
Published on: April 12, 2024
Biphasic regulation of tumorigenesis by PTK7 expression level in esophageal squamous cell carcinoma
Won-Sik Shin1, Jungsoo Gim2, Sungho Won3,4
1Department of Biochemistry, College of Life Science and Biotechnology, Yonsei University, Seoul, Republic of Korea.
Abstract:
Protein tyrosine kinase 7 (PTK7), also known as colon carcinoma kinase 4 (CCK-4), is a member of the catalytically defective receptor protein tyrosine kinase family and is upregulated in various cancers, where it is known to act as either an oncoprotein or a tumor suppressor. To understand the contrasting roles of PTK7 in tumorigenesis, we analyzed the tumorigenic characteristics of esophageal squamous cell carcinoma (ESCC) cells with low levels of endogenous PTK7 expression (TE-5 and TE-14 cells) and high levels of expression (TE-6 and TE-10 cells) after transfections with a PTK7 expression vector. PTK7 overexpression increased the proliferation of TE-5 and TE-14 cells but decreased the proliferation of TE-6 and TE-10 cells. In the ESCC cells, proliferation, migration, and invasion were initially increased and then decreased according to PTK7 expression levels, which were mirrored by initial increases and then decreases in the tyrosine phosphorylation of cellular proteins and phosphorylation of Src, Akt, and ERK. In ESCC patients included in The Cancer Genome Atlas database, those with higher PTK7 mRNA levels had a longer overall survival and lower relative risk than those with lower PTK7 mRNA levels. These results demonstrate that PTK7 biphasically regulates tumorigenesis in ESCC.
Insights
Protein tyrosine kinase 7 (PTK7) has a dual role in esophageal cancer, acting as both an oncoprotein and tumor suppressor. Higher PTK7 levels correlate with improved patient survival in esophageal squamous cell carcinoma (ESCC).
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Protein tyrosine kinase 7 (PTK7), also known as colon carcinoma kinase 4 (CCK-4), is a catalytically defective receptor tyrosine kinase.
- PTK7 exhibits varied roles in cancer, functioning as either an oncoprotein or a tumor suppressor depending on the context.
- Its expression is altered in numerous cancers, necessitating a deeper understanding of its specific functions.
Purpose of the Study:
- To investigate the biphasic role of PTK7 in esophageal squamous cell carcinoma (ESCC) tumorigenesis.
- To analyze how varying PTK7 expression levels influence ESCC cell proliferation, migration, and invasion.
- To correlate PTK7 mRNA levels with patient survival outcomes in ESCC.
Main Methods:
- Utilized PTK7 expression vector transfections in ESCC cell lines with differing endogenous PTK7 levels (TE-5, TE-14, TE-6, TE-10).
- Assessed proliferation, migration, and invasion capabilities of transfected ESCC cells.
- Measured tyrosine phosphorylation of cellular proteins and phosphorylation of key signaling molecules (Src, Akt, ERK).
- Analyzed PTK7 mRNA expression and overall survival data from The Cancer Genome Atlas (TCGA) database for ESCC patients.
Main Results:
- PTK7 overexpression differentially affected proliferation: it increased in low-expression cells (TE-5, TE-14) but decreased in high-expression cells (TE-6, TE-10).
- ESCC cell proliferation, migration, and invasion showed an initial increase followed by a decrease with rising PTK7 levels.
- These phenotypic changes were paralleled by biphasic alterations in cellular tyrosine phosphorylation and the phosphorylation of Src, Akt, and ERK.
- Higher PTK7 mRNA levels in ESCC patients were associated with significantly longer overall survival and a lower risk.
Conclusions:
- PTK7 exhibits a biphasic regulatory role in ESCC tumorigenesis, influencing cell proliferation, migration, and invasion.
- The contrasting effects of PTK7 are linked to its impact on cellular signaling pathways.
- Elevated PTK7 expression is a favorable prognostic marker in ESCC patients, suggesting a tumor-suppressive role at higher levels.
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