The molecular rationale of Src inhibition in colorectal carcinomas
Open accessAbstract
Src has been one of the most studied proto‐oncogenes. The cellular Src (c‐Src) holds a critical role in several human malignancies and has emerged as a key factor that promotes tumor progression during the multistep process of colorectal cancer (CRC) pathogenesis. The robust activation of Src in CRC of aggressive phenotype and poor prognosis seems to be a subsequent event of a strong link between its deregulated activity and the tumor's cell adhesion properties, invasiveness and metastatic potential. The rarely detected genetic defects drive interest in signaling networks that control Src kinase activity and integrate the association of Src with receptor tyrosine kinases (RTKs), such as the epidermal growth factor receptor (EGFR). Therefore, a dynamic crosstalk is being formed with oncogenic capacity and therapeutic applications, because Src inhibition seems to sensitize previously unresponsive cancer cells to chemotherapy and anti‐EGFR inhibitors. The present review explores the molecular basis behind Src inhibition in colorectal carcinomas. Furthermore, preclinical studies and clinical trials of Src inhibitors and combination regimens are discussed, providing new insights for further investigation and new therapeutic strategies.
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- Premisecitation
Inducible overexpression of mutant c-src Y527F inhibits tumor growth itself.
“inducible overexpression of the mutant c-src Y527F seems to inhibit even tumor growth itself.20”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [20] source
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- Interpretationreasoning
The mechanisms described (protein overexpression and increased kinase activity combined with apparent absence of mutations) set aberrant regulation of kinase activity as the main pathogenic mechanism of Src contribution in CRC development.
“The mechanisms described emerge as the driving force of Src deregulation in CRC, as protein overexpression and increased kinase activity combined with the apparent absence of mutations in this specific type of malignancy set the aberrant regulation of kinase activity as the main pathogenic mechanism of Src contribution in CRC development.”
Quote in the paperSubstantial claim - Premisecitation
Src inhibitors as monotherapy have not produced promising results in clinical trials.
“Up to now, Src inhibitors as a monotherapy have not produced promising results (Table 1).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites Table 1
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- Premisecitation
Csk negatively regulates c-src by phosphorylating it at the C-terminal segment.
“C-terminal src kinase (Csk) operates as a negative regulator phosphorylating c-src at the C-terminal segment (Fig. 1).22”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [22] source
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- Premisecitation
A phase II trial of dasatinib in 19 unresected and previously metastatic CRC patients was terminated due to lack of efficacy.
“a phase II trial of dasatinib in 19 unresected and previously metastatic CRC patients, who had undergone up to two prior regimens with fluoropyrimidine, oxaliplatin and irinotecan, was terminated due to lack of efficacy.83”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [83] source
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- Interpretationreasoning
Use of Src inhibitors in combination therapy regimens seems far more promising.
“The use of Src inhibitors in combination therapy regimens seems far more promising.”
Quote in the paperSubstantial claim- Rests on an assumption: Preclinical findings in CRC cell lines and mouse models predict clinical efficacy in human CRC patients.
- Premisecitation
Csk downregulated levels and kinase activity are strongly inversely correlated with upregulated c-src levels and kinase activity.
“Csk downregulated levels and kinase activity have been found to be strongly correlated inversely with upregulated c-src levels and kinase activity.23”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [23]
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- Interpretationnone given
c-src-dependent cell cycle regulation is integrated through multiple interactions with membrane receptors and their downstream mitogenic signaling pathways.
“It is now accepted that c-srcdependent cell cycle regulation is being integrated through multiple interactions with membrane receptors and their downstream mitogenic signaling pathways (Fig. 2).”
Quote in the paperSubstantial claim - Premisecitation
Src overexpression in metastatic CRC cell lines promotes tumor growth in vitro and in vivo, mainly through elevation of tyrosine phosphorylation.
“Src overexpression in metastatic CRC cell lines also seems to promote tumor growth both in vitro and in vivo targeting distinct protein substrates, respectively, mainly through elevation of tyrosine phosphorylation.15,16”
Quote in the paperSubstantial claim0 of 2 sources checked - Premisecitation
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”
Quote in the paperSubstantial claim0 of 2 sources checked - Premisecitation
Elevated c-src does not directly influence proliferation in vitro or in vivo in CRC.
“Contradictory results show that elevated c-src does not directly influence proliferation either in vitro or in vivo in CRC.47”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [47] source
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- Premisecitation
PTP1b increased expression favors higher src kinase activity by reducing Tyr530 phosphorylation.
“PTP1b increased expression favors higher levels of src kinase activity by reducing Tyr530 phosphorylation.30”
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- Premisecitation
Reduced SFK activity by molecular and pharmacological inhibition suppresses neo-vascularization in vivo through turnover of focal adhesions and VEGF/HGF-induced signaling pathways.
“Reduced SFK activity by molecular and pharmacological inhibition seems to suppress neo-vascularization in vivo.This activity takes place through turnover of focal adhesions, vascular endothelial growth factor (VEGF) and hepatocyte growth factor (HGF)-induced signaling pathways.51”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [51]
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- Premisecitation
src-like inhibition by Cbp attenuates tumor growth and invasion in CRC cells.
“src-like inhibition by Csk-binding protein (Cbp) attenuates tumor growth and invasion in CRC cells.17,18”
Quote in the paperSubstantial claim0 of 2 sources checked - Premisecitation
A conserved Src transformation fingerprint has been identified in human CRC, revealing unique expression patterns encoding transcription factors, heat shock proteins, cell growth proteins, and proliferation components.
“a conserved “Src transformation fingerprint” has been identified in human CRC, which revealed unique expression patterns encoding for transcription factors (TFs), heat shock proteins, cell growth proteins, proliferation and other cellular components.21”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [21] source
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- Premisecitation
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”
Quote in the paperSubstantial claim0 of 3 sources checked - Premisecitation
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”
Quote in the paperSubstantial claim0 of 3 sources checked - Interpretationreasoning
Src has a critical function in the invasion and metastasis of colorectal cancer.
“Given the crucial role that src plays in invasive and metastatic processes”
Quote in the paperSubstantial claim - Interpretationreasoning
Increased Src kinase activity is a potential biomarker of tumor response to therapy.
“Src increased kinase activity represents by itself a potential biomarker of the tumor' s response in therapy.”
Quote in the paperSubstantial claim - Interpretationreasoning
Src-mediated bypass of RTK inhibition is one of several mechanisms by which colorectal cancer cells become resistant to anti-EGFR targeted therapies.
“This specific capacity is one of several ways by which CRC cells acquire resistance to anti-EGFR targeted therapies”
Quote in the paperSubstantial claim - Interpretationreasoning
Src serves as an alternative bypass mechanism for RTK transactivation after RTKs are pharmacologically inhibited.
“constitutes an alternative and by-pass mechanism of RTKs transactivation after their pharmacological inhibition.”
Quote in the paperSubstantial claim - Interpretationreasoning
Preclinical studies imply that c-src inhibition may sensitize cancer cells to oxaliplatin besides anti-EGFR therapy.
“Preclinical studies imply that c-src inhibition may sensitize cancer cells to oxaliplatin besides anti-EGFR therapy.”
Quote in the paperSubstantial claim- Rests on an assumption: Preclinical findings in CRC cell lines and mouse models predict clinical efficacy in human CRC patients.
- Interpretationreasoning
Src is involved in multiple signal transduction pathways that integrate signals promoting colorectal cancer development.
“Src participates in a variety of signal transduction mechanisms integrating signals that steer the oncogenic process in CRC.”
Quote in the paperSubstantial claim - Premisecitation
A phase IB trial has shown a partial response rate of 17% in patients previously unresponsive to oxaliplatin-based chemotherapy and cetuximab when treated with dasatinib plus oxaliplatin-containing chemotherapy and cetuximab.
“a phase IB trial has already shown a partial response rate of 17% in patients that were previously unresponsive to oxaliplatin-based chemotherapy and cetuximab.92”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [92] source
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- Premisereasoning
Kras mutant colorectal tumors exhibit resistance to anti-EGFR targeted therapies.
“for example, the resistance observed in Krasmutant CRC tumors”
Quote in the paperSubstantial claim - Premisenone given
Src activates receptor tyrosine kinases such as EGFR.
“Src mediates RTKs activation, such as EGFR”
Quote in the paperSubstantial claim
- May combine two claims. 19
- Classified as probably not a substantial claim. 1
May combine two claims.
InterpretationreasoningThe transforming activity of certain CRC cells may not depend on aberrant src activity, and src activity in early-stage CRC is probably still regulated so kinase overexpression may not be active.
“This could be explained by the fact that the transforming activity of certain CRC cells may not depend upon aberrant src activity, for example KMC12 cells, whereas src activity in CRC cells of early stage is probably still regulated and kinase overexpression may not be active.”
Quote in the paperSubstantial claimMay combine two claims.
PremisecitationHigh c-src activity correlates with dismal survival and is an independent aggravating prognostic factor in CRC.
“c-src high activity was proved to be correlated with dismal survival, emerging as an independent aggravating prognostic factor.14”
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PremisecitationCsk membrane delocalization is a key event allowing SFK-dependent invasiveness in CRC cells and is associated with PAG downregulation.
“Csk membrane delocalization is a key event that allows SFKs dependent invasiveness in CRC cells and is also associated with phosphoprotein associated with glycosphingolipid-enriched microdomains downregulation (PAG).18”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [18] source
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PremisecitationCombined treatment with dasatinib and oxaliplatin in a CRC metastatic mouse model produced smaller tumors compared to single-agent therapy; oxaliplatin activates c-src through a ROS-dependent mechanism, so c-src inhibition by dasatinib sensitizes cells to oxaliplatin.
“Combined treatment with dasatinib and oxaliplatin in a CRC metastatic mouse model presented an outcome of smaller tumors compared to single-agent therapy either way.Oxaliplatin was proved to activate c-src through a ROS-dependent mechanism, thereby, c-src inhibition by dasatinib sensitized cells to oxaliplatin activity.95”
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PremisecitationCsk overexpression in highly metastatic mouse NL-17 CRC cells reduces src kinase activity in vitro and suppresses lung metastases and tumor invasiveness in vivo.
“Csk overexpression in highly metastatic mouse NL-17 CRC cells reduces src kinase activity in vitro, suppresses lung metastases and tumor invasiveness in vivo.24”
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Premisecitationc-src is implicated as a component of EGFR signal transduction, potentiating ligand-independent EGFR transactivation and facilitating EGFR phosphorylation.
“C-src has been implicated as a component of EGFR signal transduction mechanisms potentiating the receptor's transactivation, which means EGFR activation in the absence of a ligand (Fig. 2).This leads to the initiation of a series of signaling pathways linking several receptors to EGFR-dependent signaling with src facilitating EGFR phosphorylation.70”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [70]
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PremisecitationSaracatinib is an oral dual Src/Abl inhibitor targeting Csk and RTKs such as mutant EGFR; it shows anti-growth effects in several CRC cell lines in vitro and in mouse xenografts.
“Saracatinib is also an oral dual Src/Abl inhibitor targeting Csk and RTKs, such as mutant forms of EGFR.Saracatinib shows anti-growth effects in several CRC cell lines in vitro and in mouse xenografts.79”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [79] source
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Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.
Premisecitation§ The molecular rationale of Src inhibition in colorectal carcinomasc-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)”
Quote in the paperNot a substantial claim0 of 2 sources checkedMay combine two claims.
Interpretationcitationc-src is a strong mediator between EGFR and other receptors' signaling and can transactivate EGFR; therefore, pharmacological EGFR inhibition alone is insufficient to completely abrogate its activity, and combination regimens are required.
“Given the above findings, c-src is a strong mediator between EGFR and other receptors' signaling and owns the capacity of transactivating EGFR.Therefore, pharmacological inhibition of EGFR is not sufficient to completely abrogate its activity and combination regimens are required to fill in the gap.70”
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PremisecitationDasatinib is a dual oral Src/Abl inhibitor that also targets other SFK members and RTKs such as c-kit, PDGFRα/β, Ephrin receptors, and DDR1.
“Dasatinib constitutes a dual oral inhibitor of Src/V-abl Abelson murine leukemia viral oncogene homolog (Abl), which also targets a number of other SFK members and certain RTKs such as c-kit, platelet-derived growth factor-receptor a and b (PDGFRa, PDGFRb), Ephrin receptors and discoidin domain receptor 1 (DDR1).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [77] source
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Premisecitationc-src is capable of mediating EGFR-driven tumorigenesis in vivo, and EGFR/c-src interaction leads to a more aggressive tumor phenotype.
“C-src is capable of mediating EGFR-driven tumorigenesis in vivo, whereas the EGFR/c-src interaction leads to a more aggressive phenotype in tumors.73”
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Premisecitation§ The molecular rationale of Src inhibition in colorectal carcinomasAberrant c-src activation occurs in many cancer types, including CRC, where it acts as a dominant molecule at the crossroad of several signal transduction pathways, mostly RTK-driven.
“aberrant c-src activation has been described in many cancer types, among others in CRC, where it has been recognized as a dominant molecule at the crossroad of several signal transduction pathways, mostly those driven by receptor tyrosine kinases (RTKs).6”
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PremisecitationDownregulation of transmembrane PTPa inhibits src kinase activity and induces apoptosis in CRC cells.
“The downregulation of the transmembrane PTPa has been proven to inhibit src kinase activity and induce apoptosis in CRC cells.27”
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PremisecitationBosutinib, an oral Src/Abl inhibitor, abrogates c-src and FAK autophosphorylation in HT-29 cells, attenuates tumor growth in various CRC cell lines, and is active in injected nude mice.
“bosutinib, another oral Src/Abl inhibitor, which abrogated c-src and FAK autophosphorylation in HT-29 cells, attenuated tumor growth in various CRC cell lines and was found to be also active in injected nude mice.81”
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PremisecitationSplice mutants of RPTPa are detected in 30% of colon, breast, and liver tumors; expression of transforming RPTPa245 mutant facilitates src dephosphorylation/activation via RPTPa/endogenous RPTPa binding.
“splice mutants of receptor-like PTPa (RPTPa) have been detected in 30% of colon, breast and liver tumors.In particular, expression of the transforming RPTPa245 mutant in tumors facilitates the elevation of src dephosphorylation/activation via RPTPa/endogenous RPTPa binding.28”
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PremisecitationIn CRC cells, the src inhibitor SU11333 attenuates VEGF-dependent vascular permeability in mice, proving VEGF signaling is SFK-dependent.
“In CRC cells, the src inhibitor SU11333 attenuates the VEGF-dependent vascular permeability in mice proving that VEGF signaling is SFK-dependent.53”
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PremisecitationIn nude mice injected with KM12C and SW480 cells overexpressing c-src, only primary tumor growth increased, while metastatic potential in vivo and cell proliferation in vitro remained unaffected.
“in nude mice that were injected with KM12C and SW480 cells, stably transfected to overexpress c-src, only primary tumor growth was increased, whereas metastatic potential in vivo and cell proliferation in vitro remained unaffected.19”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [19]
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InterpretationreasoningSrc is not the primary tumorigenic driver but acts as a key facilitator of pathogenic molecular mechanisms in colorectal cancer.
“the emerging notion that Src does not seem to be the tumorigenic driving force rather than the key facilitator of pathogenic molecular mechanisms.”
Quote in the paperSubstantial claimMay combine two claims.
PremisecitationIn NCI-H226 lung cancer cells, c-src expression increases after long-term exposure to an EGFR inhibitory antibody; SFKs also show increased activity in cetuximab-resistant cells followed by increased sensitivity to dasatinib.
“In NCI-H226 lung cancer cells, c-src expression is increased after long-term exposure to an EGFR inhibitory antibody.SFKs also show increased activity in cetuximab-resistant cells followed by respective increased sensitivity to dasatinib.98”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [98] source
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The paper relies on this without support.
Preclinical findings in CRC cell lines and mouse models predict clinical efficacy in human CRC patients.
“These encouraging experimental data make the combination of Src/EGFR inhibition worth testing.”
The paper relies on this without support.
Kras mutations are predictive biomarkers of resistance to cetuximab in metastatic CRC.
“In metastatic CRC, Kras mutations consist of predictive biomarkers of resistance in cetuximab.”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
SRC 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 [20]
SRC plays a role in EGFR transactivation, acting as an upstream effector of EGFR in the feedback loop.
“SRC plays a role in EGFR transactivation, acting as an upstream effector of EGFR in the feedback loop [20, 43].”
From Co-targeting SRC overcomes resistance to BRAF inhibitors in colorectal cancer (2025) · cites this paper as [20]
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“This combination resulted in a subsequent decrease of several kinases downstream of Src/EGFR interaction, such as those of the bcatenin, MAPK, PI3K/mammalian target of rapamycin (mTOR) and STAT pathways.(99) These encouraging experimental data make the combination of Src/EGFR inhibition worth testing.”
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Epidermal Growth Factor Receptor Cell Proliferation Signaling Pathways
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Src inhibition blocks renal interstitial fibroblast activation and ameliorates renal fibrosis
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The Crosstalk between Src and Hippo/YAP Signaling Pathways in Non-Small Cell Lung Cancer (NSCLC)
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Self-citationThe importance of Src signaling in sarcoma
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- Authors
- Gargalionis, A. N., Karamouzis, M. V., & Papavassiliou, A. G.
- Affiliations
- National and Kapodistrian University of Athens (GR)
- Corresponding author
- Papavassiliou, Athanasios G.
- Venue
- International Journal of Cancer
- Publisher
- Wiley
- Published
- 2013-06-21
- Volume
- 134
- Issue
- 9
- Pages
- 2019-2029
- ISSN
- 0020-7136 (ISSN-L)
- 1097-0215
- OpenAlex
- W1548379836
- Cited by
- 47
- References
- 108
- Citations by year
- 2025: 2 · 2024: 1 · 2023: 6 · 2022: 3 · 2021: 6 · 2020: 7 · 2019: 2 · 2018: 2 · 2017: 4 · 2016: 5 · 2015: 5 · 2014: 3 · 2013: 1
- FWCI
- 0.69
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- International Journal of Cancer (publishedVersion)
- PubMed (publishedVersion)
- 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
- Health Sciences › Medicine › Oncology › Colorectal Cancer Treatments and Studies
- Keywords
- Src kinase, colorectal cancer, Src kinase inhibition, proto-oncogenes, tumor progression, metastasis, cell adhesion, receptor tyrosine kinase, EGFR, chemosensitization, combination therapy, Src kinase inhibitor, clinical trials
- MeSH terms
- Adenocarcinoma, Animals, Antineoplastic Agents, Clinical Trials as Topic, Humans, Colorectal Neoplasms, src-Family Kinases, Protein Kinase Inhibitors, Molecular Targeted Therapy
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