Src-family tyrosine kinases as therapeutic targets in advanced cancer
Open accessAbstract
Src-family tyrosine kinases (SFK) play critical roles in mediating many cellular pathways such as proliferation, adhesion, survival, differentiation and cell motility. There is clear evidence that SFK activity is increased in many human cancers, either through gene amplification, transcriptional upregulation, posttranslational modification by activated upstream growth factor receptors, and even in rare cases, by mutations known to increase intrinsic tyrosine kinase activity in oncoviral forms of SFK. Many recent studies using animal models of human cancer seem to indicate that SFK may only be appropriate therapeutic targets in a subset of primary tumors because of the existence of multiple independent pathways that mediate oncogenic signaling. In contrast, SFK seem to be required for specific parameters of malignant progression, such as recurrence and/or metastasis- especially involving growth in the bone microenvironment. The resulting development of SFK antagonists, and their progression through clinical trials, has brought renewed focus on this tyrosine kinase family as critical mediators of the so-called lethal phenotype of cancer.
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Preclinical evidence in sarcoma and ovarian cancer cell lines suggests that activation of Src reduces sensitivity to various chemotherapeutic drugs, including platinum agents, and that this resistance can be reversed by pharmacological inhibition.
“In addition, evidence from preclinical studies in sarcoma and ovarian cancer cell lines suggests that activation of Src reduces sensitivity to various chemotherapeutic drugs, including platinum agents, and that this resistance can be reversed by pharmacological inhibition [19, 20][21–23][24].”
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 [20]
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BindingDB Entry 50018463: Allosteric inhibitors of the STAT3 signaling pathway.
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- Authors
- Gelman, I. H.
- Affiliations
- Roswell Park Comprehensive Cancer Center (US)
- Corresponding author
- Gelman, Irwin H
- ORCID
- Gelman, Irwin H
- Venue
- Frontiers in Bioscience
- Publisher
- IMR Press
- Published
- 2011
- Volume
- E3
- Issue
- 3
- Pages
- 801-807
- ISSN
- 1944-7892 (ISSN-L)
- 1945-0494
- 1945-0508
- DOI
- 10.2741/e287
- OpenAlex
- W2342671164
- Cited by
- 28
- References
- 76
- Citations by year
- 2026: 2 · 2024: 1 · 2023: 2 · 2022: 1 · 2021: 1 · 2020: 1 · 2019: 1 · 2018: 1 · 2017: 3 · 2016: 3 · 2015: 1 · 2014: 3 · 2013: 2 · 2012: 5
- FWCI
- 0.44
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Frontiers in Bioscience-Elite (publishedVersion)
- PubMed (publishedVersion)
- Funders
- U.S. Department of Defense (W81XWH)
- National Institutes of Health (W81XWH)
- National Cancer Institute (CA094108, R01CA116430, CA116430)
- 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 family kinases, therapeutic target, advanced cancer, oncogenic signaling, metastasis, bone microenvironment, tumor recurrence, malignant progression, gene amplification, clinical trials
- MeSH terms
- Antineoplastic Agents, Humans, Neoplasms, src-Family Kinases, Protein Kinase Inhibitors
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