Related Experiment Video
Updated: Jun 20, 2026

A Method for Screening and Validation of Resistant Mutations Against Kinase Inhibitors
Published on: December 7, 2014
Src kinases as therapeutic targets for cancer
Lori C Kim1, Lanxi Song, Eric B Haura
1University of South Florida College of Medicine, Tampa, FL, USA.
Abstract:
Src family kinases (SFKs) have a critical role in cell adhesion, invasion, proliferation, survival, and angiogenesis during tumor development. SFKs comprise nine family members that share similar structure and function. Overexpression or high activation of SFKs occurs frequently in tumor tissues and they are central mediators in multiple signaling pathways that are important in oncogenesis. SFKs can interact with tyrosine kinase receptors, such as EGFR and the VEGF receptor. SFKs can affect cell proliferation via the Ras/ERK/MAPK pathway and can regulate gene expression via transcription factors such as STAT molecules. SFKs can also affect cell adhesion and migration via interaction with integrins, actins, GTPase-activating proteins, scaffold proteins, such as p130(CAS) and paxillin, and kinases such as focal adhesion kinases. Furthermore, SFKs can regulate angiogenesis via gene expression of angiogenic growth factors, such as fibroblast growth factor, VEGF, and interleukin 8. On the basis of these important findings, small-molecule SFK inhibitors have been developed and are undergoing early phase clinical testing. In preclinical studies these agents can suppress tumor growth and metastases. The agents seem to be safe in humans and could add to the therapeutic arsenal against subsets of cancers.
Insights
Src family kinases (SFKs) are crucial in cancer development and spread. Small-molecule inhibitors targeting SFKs show promise in preclinical studies and early human trials for cancer treatment.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Src family kinases (SFKs) are implicated in key cancer processes including cell adhesion, invasion, proliferation, survival, and angiogenesis.
- SFKs are frequently overexpressed or highly activated in tumor tissues, playing a central role in oncogenic signaling pathways.
- SFKs interact with various cellular components, including tyrosine kinase receptors (e.g., EGFR, VEGF receptor), integrins, and other signaling molecules.
Purpose of the Study:
- To review the critical role of SFKs in tumor development and progression.
- To highlight the molecular mechanisms by which SFKs influence cancer hallmarks.
- To discuss the therapeutic potential of small-molecule SFK inhibitors in cancer treatment.
Main Methods:
- Literature review of studies on SFK function in cancer.
- Analysis of signaling pathways regulated by SFKs, including Ras/ERK/MAPK and STAT pathways.
- Examination of SFK interactions with cellular adhesion molecules and angiogenic factors.
- Review of preclinical and early clinical data for small-molecule SFK inhibitors.
Main Results:
- SFKs regulate cell proliferation, gene expression, cell adhesion, migration, and angiogenesis through diverse molecular interactions.
- SFKs modulate signaling pathways involving growth factors like VEGF and fibroblast growth factor.
- Small-molecule SFK inhibitors have demonstrated efficacy in suppressing tumor growth and metastasis in preclinical models.
- SFK inhibitors appear safe in human trials, suggesting potential as a cancer therapeutic.
Conclusions:
- SFKs are vital mediators in multiple oncogenic signaling pathways, contributing to tumor development and metastasis.
- Targeting SFKs with small-molecule inhibitors represents a promising therapeutic strategy for various cancers.
- SFK inhibitors have shown safety and efficacy in preclinical and early clinical studies, warranting further investigation.
Related Concept Videos
Transducer Mechanism: Enzyme-Linked Receptors
Major types that are helpful drug targets include:
Targeted Cancer Therapies
There are several types of targeted therapies against specific...
Targeted Cancer Therapies
There are several types of targeted therapies against specific...
M-Cdk Drives Transition Into Mitosis
Cyclin-dependent kinases, or Cdks, work in concert with cyclins to control cell cycle transitions. M-Cdk, a complex of Cdk1 bound to M cyclin, is a well-known example of this coordinated control that drives the transition from the G2 to the M phase.
M cyclin...
mTOR Signaling and Cancer Progression
The mTOR pathway or the...
mTOR Signaling and Cancer Progression
The mTOR pathway or the...
