ArticleOncogene2008
Decreased CHK protein levels are associated with Src activation in colon cancer cells.
Article in Oncogene, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 26 citations in OpenAlex.
- MMP-2 regulates Src activation via repression of the CHK/MATK tumor suppressor in osteosarcoma.Cancer reports (Hoboken, N.J.) · 2023Article
- Regulation, targets and functions of CSK.Frontiers in cell and developmental biology · 2023Review
- Dissection of the catalytic and regulatory structure-function relationships of Csk protein tyrosine kinase.Frontiers in cell and developmental biology · 2023Review
- Regulation, targets and functions of CHK.Frontiers in cell and developmental biology · 2022Review
- Article
- CHK Methylation Is Elevated in Colon Cancer Cells and Contributes to the Oncogenic Properties.Frontiers in cell and developmental biology · 2021Article
- Regulation of Src Family Kinases during Colorectal Cancer Development and Its Clinical Implications.Cancers · 2020Review
- Epigenome-Wide Association Study for All-Cause Mortality in a Cardiovascular Cohort Identifies Differential Methylation in Castor Zinc Finger 1 (Journal of the American Heart Association · 2019Article
- Defining UHRF1 Domains that Support Maintenance of Human Colon Cancer DNA Methylation and Oncogenic Properties.Cancer cell · 2019Article
- Csk-homologous kinase (Chk) is an efficient inhibitor of Src-family kinases but a poor catalyst of phosphorylation of their C-terminal regulatory tyrosine.Cell communication and signaling : CCS · 2017Article
- Article
- Methylation profiling identifies 2 groups of gliomas according to their tumorigenesis.Neuro-oncology · 2011Article
- Src family tyrosine kinases-driven colon cancer cell invasion is induced by Csk membrane delocalization.Oncogene · 2010Article
- Acetylcholine-induced activation of M3 muscarinic receptors stimulates robust matrix metalloproteinase gene expression in human colon cancer cells.American journal of physiology. Gastrointestinal and liver physiology · 2009Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Src activation has been associated with colon cancers but the mechanism underlying Src activation is largely unknown. Csk-homologous kinase (CHK) can inhibit the kinase activity of certain Src kinase family members in vitro by phosphorylating the C-terminal tyrosine and by a non-catalytic mechanism. CHK was previously reported to be expressed primarily in brain and hematopoietic cells. We report herein that CHK is also expressed in normal colon cell lines. Furthermore, CHK protein levels are significantly decreased in various colon cancer cell lines and the decrease correlates with the increased specific activity of Src in these cell lines, while the level of the other Src inhibitory kinase, C-terminal Src kinase, is not significantly changed. CHK is also expressed in normal colon tissues but its expression level is decreased in colon cancer tissues collected from the same patients. Immunofluorescence microscopy shows that CHK colocalizes with Src in normal colon FHC cells. Overexpression of CHK in colon cancer cells results in inactivation of Src without phosphorylating Y530 at its C-terminus. In addition, CHK suppresses anchorage-independent cell growth and cell invasion of colon cancer cells. These results reveal a potentially important role for CHK in Src activation and tumorigenicity in colon cancer cells.
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