The DOI matches its Crossref record; 171 of the 171 references it cites were found in a registry or an index.
Src family kinases in tumor progression and metastasis
Abstract
The Src family of non-receptor protein tyrosine kinases plays critical roles in a variety of cellular signal transduction pathways, regulating such diverse processes as cell division, motility, adhesion, angiogenesis, and survival. Constitutively activated variants of Src family kinases, including the viral oncoproteins v-Src and v-Yes, are capable of inducing malignant transformation of a variety of cell types. Src family kinases, most notably although not exclusively c-Src, are frequently overexpressed and/or aberrantly activated in a variety of epithelial and non-epithelial cancers. Activation is very common in colorectal and breast cancers, and somewhat less frequent in melanomas, ovarian cancer, gastric cancer, head and neck cancers, pancreatic cancer, lung cancer, brain cancers, and blood cancers. Further, the extent of increased Src family activity often correlates with malignant potential and patient survival. Activation of Src family kinases in human cancers may occur through a variety of mechanisms and is frequently a critical event in tumor progression. Exactly how Src family kinases contribute to individual tumors remains to be defined completely, however they appear to be important for multiple aspects of tumor progression, including proliferation, disruption of cell/cell contacts, migration, invasiveness, resistance to apoptosis, and angiogenesis. This review details the evidence for Src family activation in human tumors, and emphasizes possible consequences to tumor progression. Given the ability of Src and its family members to participate in so many aspects of tumor progression and metastasis, Src family kinases are attractive targets for future anti-cancer therapeutics.
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“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 [22]
In the citing paper
“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 [22]
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Metadata
- Authors
- Summy, J. M., & Gallick, G. E.
- Affiliations
- The University of Texas MD Anderson Cancer Center (US)
- Corresponding author
- Gallick, Gary E.
- Venue
- Cancer and Metastasis Reviews
- Published
- 2003-12
- Volume
- 22
- Issue
- 4
- Pages
- 337-358
- ISSN
- 0167-7659 (ISSN-L)
- 1573-7233
- OpenAlex
- W1589166971
- Cited by
- 827
- References
- 171
- Citations by year
- 2026: 15 · 2025: 15 · 2024: 17 · 2023: 17 · 2022: 26 · 2021: 27 · 2020: 26 · 2019: 35 · 2018: 32 · 2017: 28 · 2016: 32 · 2015: 37 · 2014: 64 · 2013: 55 · 2012: 49
- FWCI
- 4.32
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- Locations
- Cancer and Metastasis Reviews (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (5r01ca065527-07)
- National Cancer Institute (U54CA090810, 2 R01 CA65527)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › 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 › Mechanisms of cancer metastasis
- Keywords
- Src family kinases, Src kinase, non-receptor tyrosine kinase, tumor progression, metastasis, constitutive kinase activation, v-Src, malignant transformation, cell migration and invasion, angiogenesis, apoptosis resistance, cancer therapeutics, colorectal cancer, breast cancer, melanoma, lung cancer
- MeSH terms
- Enzyme Activation, Humans, Neoplasm Metastasis, Neoplasms, Neovascularization, Pathologic, Signal Transduction, Disease Progression, src-Family Kinases
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