Dataset Information

Biphasic regulation of tumorigenesis by PTK7 expression level in esophageal squamous cell carcinoma.

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.

SUBMITTER: Shin WS

PROVIDER: S-EPMC5986804 | biostudies-literature | 2018 Jun

REPOSITORIES: biostudies-literature

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Biphasic regulation of tumorigenesis by PTK7 expression level in esophageal squamous cell carcinoma.

Shin Won-Sik WS Gim Jungsoo J Won Sungho S Lee Seung-Taek ST

Scientific reports 20180604 1

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 cell ...[more]

PMID: 29867084

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Project description:p33(ING1b), a newly discovered candidate tumor suppressor gene and a nuclear protein, belongs to the inhibitor of growth gene family. Previous studies have shown that p33(ING1b) is involved in the restriction of cell growth and proliferation, apoptosis, tumor anchorage-independent growth, cellular senescence, maintenance of genomic stability and modulation of cell cycle checkpoints. Loss of nuclear p33(ING1b) has been observed in melanoma, seminoma, papillary thyroid carcinoma, oral squamous cell carcinoma, breast ductal cancer and acute lymphoblastic leukemia. Inactivation and/or decreased expression of p33(ING1b) have been reported in various types of cancer, including head and neck squamous cell, breast, lung, stomach, blood and brain malignancies. Since little is known about the clinicopathological significance of p33(ING1b) in esophageal squamous cell carcinoma (ESCC), this study aimed to investigate the association of p33(ING1b) expression with clinicopathological variables and particularly interesting new cysteine-histidine rich protein (PINCH) in patients with ESCC. p33(ING1b) expression was examined by immunohistochemistry in 20 normal esophageal mucosa and in 64 ESCC specimens. The results revealed that the positive expression of p33(ING1b) protein in normal squamous cells was localized in the nucleus alone and the positive rate was 95%, while in ESCCs, the positive expression was mainly in the cytoplasm, together with nuclear expression, and the positive rate was 36% (P<0.0001). Furthermore, the cases with lymph node metastasis showed a higher frequency of positive cytoplasmic expression than those without metastasis (P=0.001). The cytoplasmic expression of p33(ING1b) was positively related to PINCH expression (P<0.0001) in ESCC, and the cases positive for both proteins had a high lymph node metastasis rate (P=0.001). In conclusion, p33(ING1b) cellular compartmental shift from the nucleus to the cytoplasm may cause loss of normal cellular function and play a central role in the tumorigenesis and metastasis of ESCC.

Dataset Information

Biphasic regulation of tumorigenesis by PTK7 expression level in esophageal squamous cell carcinoma.

Publications

Biphasic regulation of tumorigenesis by PTK7 expression level in esophageal squamous cell carcinoma.

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