Increase in activity and level of pp60c-src in progressive stages of human colorectal cancer.
Open accessAbstract
Activation of the tyrosine kinase of the c-src gene product, pp60c-src, has been shown to occur in nearly every primary colorectal carcinoma, and is found as early as in polyps of high malignant potential. However, no studies have addressed potential pp60c-src changes which occur during progression. To examine this question, we have studied kinase activity and protein levels in 7 colonic polyps, 19 primary lesions, and 19 liver metastases relative to normal colonic mucosa. Significant increases in tyrosine kinase activity were seen as early as in colonic polyps of high malignant potential. Further increases were observed in activity and level in primary tumors. However, the greatest increases in activity and protein levels were observed in liver metastases. Additionally, six metastatic lesions were obtained in which synchronous primary tumor was resected. In each of these liver metastases, pp60c-src activity and level were significantly increased relative to the corresponding primary tumor, as well as to normal colonic mucosa. Our results demonstrate that progression of colon primary tumors to liver metastases correlates with increased pp60c-src kinase activity and protein level.
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The SRC activation signature score was significantly associated with metastasis and primary tumor stage I-IV progression.
“Moreover, the SRC activation signature score was significantly associated with metastasis and primary tumor stage I-IV progression (Fig. 2g,h), in agreement with previous studies in CRC [37–40].”
From An integrative gene expression signature analysis identifies CMS4 KRAS-mutated colorectal cancers sensitive to combined MEK and SRC targeted therapy (2022) · cites this paper as [40]
The Results report higher pp60c-src activity and protein levels in liver metastases, supporting the metastasis part of the claimed agreement. But the same section says there were no significant differences in primary-tumor activity by Dukes’ stage, so this paper does not support an association with primary-tumor stage I–IV progression. It measured pp60c-src activity and levels, not the citing paper’s signature score. (LLM, conf=0.88)
Experimental — accuracy not yet measuredColon cancer progression may be dependent on increased Src family kinase protein level and subsequent activity.
“Talamonti et al reported increased activity and expression of SFKs in progressive stages of human colorectal cancer, suggesting that colon cancer progression may be dependent on increased SFK protein level and subsequent activity (Talamonti et al., 1993).”
From Dasatinib sensitizes KRAS mutant colorectal tumors to cetuximab (2011) · cites this paper as Talamonti et al., 1993
The Results report increasing pp60c-src protein levels and kinase activity across progressive stages of colorectal cancer, and the Discussion suggests elevated activity may contribute to metastatic progression (pages not supplied). But the study examines c-src specifically, not Src-family kinases as a group; it also says the increased activity cannot be explained solely by increased protein level and does not establish that one subsequently causes the other. (LLM, conf=0.85)
Experimental — accuracy not yet measuredSRC expression and activity are higher in primary colon tumors than in benign polyps or non-transformed colonic mucosa, and SRC activity increases in progressive stages of colorectal cancer.
“Higher expression and activity of SRC has been documented in primary colon tumors compared with benign polyps or non-transformed colonic mucosa, and increased activity is observed in progressive stages of CRC [23–26].”
From Co-targeting SRC overcomes resistance to BRAF inhibitors in colorectal cancer (2025) · cites this paper as [25]
c-Src expression and activity increase in CRC liver metastases compared with metastases derived from other tumor types.
“However, c-Src seems to experience a robust increase in expression and activity in CRC liver metastases compared with metastases derived from other tumors types [11, 12]”
From Dasatinib, a Src inhibitor, sensitizes liver metastatic colorectal carcinoma to oxaliplatin in tumors with high levels of phospho-Src (2016) · cites this paper as [12]
c-src expression and activity are robustly increased in CRC liver metastases compared to metastases from other tumor types.
“C-src, though, seems to have a robust increase regarding expression and activity in CRC liver metastases compared to those derived from other tumors types.3,11,13”
From The molecular rationale of Src inhibition in colorectal carcinomas (2014) · cites this paper as [11]
In CRC cell lines and primary tumors, c-src kinase activity and protein expression are elevated compared to normal colonic mucosal cells/fibroblasts or normal adjacent tissue.
“In CRC cell lines and primary tumors, both c-src kinase activity and protein expression levels have been found elevated compared either to normal colonic mucosal cells and fibroblasts or normal adjacent tissue, respectively.3,10,11”
From The molecular rationale of Src inhibition in colorectal carcinomas (2014) · cites this paper as [11]
Increased c-src specific activity and expression are detected in colonic polyps of high malignant potential and severe dysplasia.
“Increased specific activity and expression levels have been detected in colonic polyps of high malignant potential and severe dysplasia.11,12”
From The molecular rationale of Src inhibition in colorectal carcinomas (2014) · cites this paper as [11]
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- Authors
- Talamonti, M. S., Roh, M. S., Curley, S. A., & Gallick, G. E.
- Affiliations
- The University of Texas MD Anderson Cancer Center (US)
- ORCID
- Talamonti, M S
- Venue
- Journal of Clinical Investigation
- Published
- 1993-01-01
- Volume
- 91
- Issue
- 1
- Pages
- 53-60
- ISSN
- 0021-9738 (ISSN-L)
- PMC
- PMC329994
- OpenAlex
- W2030565228
- Cited by
- 399
- References
- 45
- Citations by year
- 2026: 1 · 2025: 3 · 2024: 4 · 2023: 11 · 2022: 6 · 2021: 6 · 2020: 6 · 2019: 6 · 2018: 6 · 2017: 14 · 2016: 8 · 2015: 13 · 2014: 11 · 2013: 17 · 2012: 24
- FWCI
- 2.45
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Clinical Investigation (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (5r01ca053167-06)
- National Cancer Institute (CA09599, CA53167, T32CA009599)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
- Health Sciences › Medicine › Pathology and Forensic Medicine › Cancer Mechanisms and Therapy
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mechanisms of cancer metastasis
- Keywords
- Src kinase, tyrosine kinase activity, colorectal cancer, tumor progression, colonic polyps, liver metastasis, synchronous primary tumors, oncogene activation
- MeSH terms
- Adenocarcinoma, Adenoma, Antigen-Antibody Complex, Colonic Neoplasms, Colonic Polyps, Humans, Intestinal Mucosa, Liver Neoplasms, Neoplasm Metastasis, Neoplasm Staging, Phosphopyruvate Hydratase, Phosphorylation, Protein Kinases, Protein-Tyrosine Kinases, Rectal Neoplasms, Reference Values, Immunoblotting, Proto-Oncogene Proteins pp60(c-src)
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