The Role of Src in Solid Tumors
Open accessAbstract
The proto-oncogene c-Src (Src) encodes a nonreceptor tyrosine kinase whose expression and activity are correlated with advanced malignancy and poor prognosis in a variety of human cancers. Nine additional enzymes with homology to Src have been identified and collectively are referred to as Src family kinases (SFKs). Together, SFKs represent the largest family of nonreceptor tyrosine kinases and interact directly with receptor tyrosine kinases, G-protein-coupled receptors, steroid receptors, signal transducers and activators of transcription, and molecules involved in cell adhesion and migration. These interactions lead to a diverse array of biological functions including proliferation, cell growth, differentiation, cell shape, motility, migration, angiogenesis, and survival. Studies investigating mutational activation of Src in human cancers suggest that this may be a rare event and that wild-type Src is weakly oncogenic. Thus, the role of Src in the development and progression of human cancer remains unclear. Recently, it was suggested that increased SFK protein levels and, more importantly, SFK tyrosine kinase activity are linked to cancer progression and metastatic disease by facilitating the action of other signaling proteins. This accumulating body of evidence indicates that SFKs may represent a promising therapeutic target for the treatment of solid tumors. This review discusses the role of SFKs in solid tumors and the recent therapeutic advances aimed at targeting this family of tyrosine kinases in cancer.
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SRC kinases can directly modulate many downstream targets including c-MYC, related to drug resistance and tumor cell survival.
“In addition to MAPK, SRC kinases can directly modulate many downstream targets including and c-MYC [19, 21, 22, 44], related to drug resistance and tumor cell survival.”
From Co-targeting SRC overcomes resistance to BRAF inhibitors in colorectal cancer (2025) · cites this paper as [21]
The ‘Src Family Kinases Structure and Activation’ section says Src interacts with several signaling proteins and regulates survival. The pancreatic- and colorectal-cancer sections also link Src signaling to drug resistance. But the copy does not identify c-MYC as a Src target or establish that Src directly modulates it. (LLM, conf=0.88)
Experimental — accuracy not yet measuredSRC kinase has been implicated in the development and progression of cancer.
“SRC kinase, a cytoplasmic non-receptor tyrosine kinase, has been implicated in the development and progression of cancer [19–22].”
From Co-targeting SRC overcomes resistance to BRAF inhibitors in colorectal cancer (2025) · cites this paper as [21]
c-Src is a 60-kD non-receptor protein tyrosine kinase and a member of the 9-gene Src family kinases.
“The c-src is a non-receptor protein tyrosine kinase with a 60-kD molecular weight.It is a member of a 9-gene family named the Src family kinases (SFKs)”
From The molecular rationale of Src inhibition in colorectal carcinomas (2014) · cites this paper as [2]
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src Expression in Small-Cell Lung Carcinoma and Other Neuroendocrine Malignancies
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Survey of Src activity and Src-related growth and migration in prostate cancer lines
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Phase I open-labeled trial of gemcitabine and dasatinib in advanced solid tumors
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Flagged first, then by citations
Research works printed but not linked: 1
- [47]Kopetz S Wu J Davies M Synergistic effects of combination therapy with anti-EGFR and anti-Src therapy in vitro in colon cancer 2007 Gastrointestinal Cancers Symposium Abstract 406
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Molecular targeted therapy for anticancer treatment
Min, H.-Y., & Lee, H.-Y. (2022) · Experimental & Molecular Medicine · doi:10.1038/s12276-022-00864-3 · Cited by 569 · see citing works
Leveraging Uncertainty in Machine Learning Accelerates Biological Discovery and Design
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“These kinases have well-documented roles in cancer, immunological, or infectious disease (Ali et al., 2014; Lougheed et al., 2011; Wang et al., 2009; Wheeler et al., 2009).”
BackgroundSrc Family Kinases as Therapeutic Targets in Advanced Solid Tumors: What We Have Learned So Far
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Src family kinases and paclitaxel sensitivity
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The molecular rationale of Src inhibition in colorectal carcinomas
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Src-family tyrosine kinases as therapeutic targets in advanced cancer
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Activation of Src and transformation by an RPTPα splice mutant found in human tumours
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Co-targeting SRC overcomes resistance to BRAF inhibitors in colorectal cancer
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- Authors
- Wheeler, D. L., Iida, M., & Dunn, E. F.
- Affiliations
- University of Wisconsin–Madison (US)
- Corresponding author
- Wheeler, Deric L.
- Venue
- The Oncologist
- Publisher
- Oxford University Press (OUP)
- Published
- 2009-07-01
- Volume
- 14
- Issue
- 7
- Pages
- 667-678
- ISSN
- 1083-7159 (ISSN-L)
- 1549-490X
- PMC
- PMC3303596
- OpenAlex
- W2132663758
- Cited by
- 346
- References
- 103
- Citations by year
- 2026: 14 · 2025: 17 · 2024: 16 · 2023: 17 · 2022: 18 · 2021: 29 · 2020: 28 · 2019: 18 · 2018: 16 · 2017: 27 · 2016: 18 · 2015: 17 · 2014: 27 · 2013: 17 · 2012: 18
- FWCI
- 2.64
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- academic.oup.com/journals/pages/open_access/funder_policies/chorus/standard_publication_model (vor)
- Locations
- The Oncologist (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Bristol-Myers Squibb
- Topics
- Health Sciences › Medicine › Pathology and Forensic Medicine › Cancer Mechanisms and Therapy
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Tyrosine Phosphatases
- Keywords
- Src kinase, Src family kinases, non-receptor tyrosine kinase, solid tumors, tumor progression, metastasis, kinase inhibitors, therapeutic target, oncogenic signaling, cell migration, angiogenesis
- MeSH terms
- Proto-Oncogene Mas, Animals, Humans, Neoplasms, Drug Delivery Systems, src-Family Kinases, Protein Kinase Inhibitors
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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