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Cited by 158Cell Adhesion Molecules ResearchCellular Mechanics and InteractionsProtein Kinase Regulation and GTPase Signaling

Focal adhesion kinase: from biological functions to therapeutic strategies

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Tan, Ximin, Yan, Yuheng, Song, Bin, Zhu, Shuangli, Mei, Qi, Wu, Kongming·2023·Experimental Hematology & Oncology
DOI 10.1186/s40164-023-00446-7PMC PMC10519103
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Abstract

Focal adhesion kinase (FAK), a nonreceptor cytoplasmic tyrosine kinase, is a vital participant in primary cellular functions, such as proliferation, survival, migration, and invasion. In addition, FAK regulates cancer stem cell activities and contributes to the formation of the tumor microenvironment (TME). Importantly, increased FAK expression and activity are strongly associated with unfavorable clinical outcomes and metastatic characteristics in numerous tumors. In vitro and in vivo studies have demonstrated that modulating FAK activity by application of FAK inhibitors alone or in combination treatment regimens could be effective for cancer therapy. Based on these findings, several agents targeting FAK have been exploited in diverse preclinical tumor models. This article briefly describes the structure and function of FAK, as well as research progress on FAK inhibitors in combination therapies. We also discuss the challenges and future directions regarding anti-FAK combination therapies.

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  • Non-receptor tyrosine kinases such as FAK and SRC can promote resistance to KRAS-targeted therapy.

    “In addition to RTKs, non-receptor tyrosine kinases such as focal adhesion kinase (FAK) and SRC can promote resistance to KRAS-targeted therapy.”

    From Differential Response and Resistance to KRAS-Targeted Therapy (2025) · cites this paper as [146]

    In “Combination with targeted therapies” (page not provided), the review says that targeting FAK–YAP signaling with IN10018 may prevent resistance to KRAS G12C inhibitors. It does not establish that SRC promotes resistance to KRAS-targeted therapy, and its FAK discussion is specific to KRAS G12C inhibition. (LLM, conf=0.86)

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Cited by

Sorted by citations

Authors
Tan, X., Yan, Y., Song, B., Zhu, S., Mei, Q., & Wu, K.
Affiliations
  • Tongji Hospital (CN)
  • Shanxi Medical University (CN)
Corresponding author
  • Mei, Qi
  • Wu, Kongming
ORCID
Venue
Experimental Hematology & Oncology
Publisher
Springer Science and Business Media LLC
Published
2023-09-25
Volume
12
Issue
1
Pages
83-83
ISSN
2162-3619 (ISSN-L)
DOI
10.1186/s40164-023-00446-7
PMC
PMC10519103
OpenAlex
W4387020789
Cited by
158
References
3
Citations by year
2026: 47 · 2025: 66 · 2024: 44 · 2023: 1
FWCI
6.14
Type
journal article
Language
en
Open access
Licence
Locations
  • Experimental Hematology and Oncology (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
National Natural Science Foundation of China (82272794)
Topics
  • Health Sciences › Medicine › Immunology and Allergy › Cell Adhesion Molecules Research
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Cellular Mechanics and Interactions
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
Keywords
focal adhesion kinase, FAK inhibitors, combination therapy, cancer stem cells, tumor microenvironment, metastasis, cell proliferation and migration, non-receptor tyrosine kinase

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