Comparative tyrosine-kinase profiles in colorectal cancers: Enhanced arg expression in carcinoma as compared with adenoma and normal mucosa

Chen, Wei Shone; Kung, Hsing Jien; Yang, Wen; Lin, Wen-chang

doi:10.1002/(sici)1097-0215(19991126)83:5<579::aid-ijc1>3.0.co;2-r

Cited by 72 publications

(51 citation statements)

References 15 publications

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“…Changes in the activation of the Abl kinases also may modulate cell-cell adhesion during tumor progression and metastasis. In this regard, enhanced expression of Abl or Arg has been reported in a subset of metastatic colon carcinomas, pancreatic ductal carcinoma, and renal medullary carcinoma (40)(41)(42). Excessive Abl/Arg kinase activity may disturb the proper balance of Rho and Rac activation and induce altered cytoskeletal reorganization, thereby affecting cell-cell adhesion.…”

Section: Discussionmentioning

confidence: 99%

Abl tyrosine kinases regulate cell–cell adhesion through Rho GTPases

Zandy

Playford

Pendergast

2007

Proc. Natl. Acad. Sci. U.S.A.

119

132

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Section: Discussionmentioning

confidence: 99%

Abl tyrosine kinases regulate cell–cell adhesion through Rho GTPases

Zandy

Playford

Pendergast

2007

Proc. Natl. Acad. Sci. U.S.A.

119

132

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“…40 However, more recent work has also reported significant expression in colon and prostate cancer. [41][42][43] In contrast, Fyn expression was restricted to the isogenic SW480 and SW620 cell lines. Most surprising, however, was the considerable variation seen in the pattern of SFK members expressed within different cell lines.…”

Section: Discussionmentioning

confidence: 99%

Src family kinase members have a common response to histone deacetylase inhibitors in human colon cancer cells

Hirsch

Smith-Windsor

Bonham

2005

Intl Journal of Cancer

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Histone deacetylase inhibitors (HDIs) induce cell cycle arrest, differentiation and/or apoptosis in numerous cancer cell types and have shown promise in clinical trials. These agents are particularly novel, given their ability to selectively influence gene expression. Previously, we demonstrated that the HDIs butyrate and trichostatin A (TSA) directly repress c-Src proto-oncogene expression in many cancer cell lines. Activation and/or overexpression of c-Src have been frequently observed in numerous malignancies, especially of the colon. Therefore, our observation was particularly interesting since butyrate is a naturally abundant component of the large intestine and has been suggested to be a cancer-preventive agent. However, c-Src is not the only Src family kinase (SFK) member to be implicated in the development of human cancers, including those of the colon. Therefore, the relative expression levels of known SFKs were examined in a panel of human colon cancer cell lines. We found a surprisingly diverse expression pattern but noted that most cell lines expressed relatively high levels of at least 2 SFKs. When the effects of butyrate and TSA were examined in representative cell lines, the expression of all SFKs was repressed in a dose-and time-dependent manner. Further, detailed examination of Lck, Yes and Lyn demonstrated that this repression had a direct effect on transcription and was independent of new protein synthesis. These results mirror our earlier data obtained with c-Src and suggest that SFKs are a major target of HDIs and likely account in part for the anticancer effects of these promising new drugs. ' 2005 Wiley-Liss, Inc.

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“…Though the study demonstrated a positive and differential RON expression in tumors derived from primary CRC patients it failed to detect any changes in the RON transcript in secondary colon metastasis using RT-PCR based approach [46]. Previous studies have emphasized RON is implicated in metastatic phenotype of CRC.…”

Section: Oncogenic Potential Of Ronmentioning

confidence: 73%

“…In another study a comprehensive transcriptional profiling of RON and other kinases was done in different CRC stages -normal colon mucosa, adenomatous polyps, primary carcinoma and secondary metastases [46]. Though the study demonstrated a positive and differential RON expression in tumors derived from primary CRC patients it failed to detect any changes in the RON transcript in secondary colon metastasis using RT-PCR based approach [46].…”

Section: Oncogenic Potential Of Ronmentioning

confidence: 99%

RON - The Con in Colorectal Carcinoma

Tarang

Wang²

2012

TOCOLCJ

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Abstract:The recepteur d'origine nantais (RON) is a member of MET family of receptor tyrosine kinase (RTKs), an overexpression of which has been observed in several cancers. The expression of RON gene is required during embryonic development and also plays critical roles in regulating macrophage inflammatory response. In CRC, the overexpression of moderate RON activity contributes to their oncogenic potential by regulating several key processes such as proliferation, motility and resistance to apoptosis. Interestingly, an aberrant RON expression is often associated with the generation of several splice variants with unique transforming activities. The targeting of RON signaling pathway by the use of monoclonal antibodies and small-molecule inhibitors has shown promising therapeutic results in animal models. The present article aims at summarizing the current understanding of RON kinase in CRC.

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Comparative tyrosine-kinase profiles in colorectal cancers: Enhanced arg expression in carcinoma as compared with adenoma and normal mucosa

Cited by 72 publications

References 15 publications

Abl tyrosine kinases regulate cell–cell adhesion through Rho GTPases

Abl tyrosine kinases regulate cell–cell adhesion through Rho GTPases

Src family kinase members have a common response to histone deacetylase inhibitors in human colon cancer cells

RON - The Con in Colorectal Carcinoma

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