ArticleFrontiers in oncology2019
Inhibition of FAK Signaling Elicits Lamin A/C-Associated Nuclear Deformity and Cellular Senescence.
Article in Frontiers in oncology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 32 citations in OpenAlex.
- Inhibition of integrin binding to ligand arg-gly-asp motif induces AKT-mediated cellular senescence in hepatic stellate cells.Molecular and cellular biochemistry · 2024Article
- Article
- Simultaneous inhibition of FAK and ROS1 synergistically repressed triple-negative breast cancer by upregulating p53 signalling.Biomarker research · 2024Article
- Review
- Focal adhesion kinase: from biological functions to therapeutic strategies.Experimental hematology & oncology · 2023Review
- On the Value of In Vitro Cell Systems for Mechanobiology from the Perspective of Yes-Associated Protein/Transcriptional Co-Activator with a PDZ-Binding Motif and Focal Adhesion Kinase and Their Involvement in Wound Healing, Cancer, Aging, and Senescence.International journal of molecular sciences · 2023Review
- SEMA6C: a novel adhesion-independent FAK and YAP activator, required for cancer cell viability and growth.Cellular and molecular life sciences : CMLS · 2023Article
- Genome-wide screening for genetic variants in polyadenylation signal (PAS) sites in mouse selection lines for fatness and leanness.Mammalian genome : official journal of the International Mammalian Genome Society · 2023Article
- Overview of cellular homeostasis-associated nuclear envelope lamins and associated input signals.Frontiers in cell and developmental biology · 2023Review
- Gaussian curvature-driven direction of cell fate toward osteogenesis with triply periodic minimal surface scaffolds.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Lung transcriptome of nonhuman primates exposed to total- and partial-body irradiation.Molecular therapy. Nucleic acids · 2022Article
- Lamin-A/C Is Modulated by the Involvement of Histamine-Mediated Calcium/Calmodulin-Dependent Kinase II in Lung Cancer Cells.International journal of molecular sciences · 2022Article
- FAK Executes Anti-Senescence via Regulating EZH2 Signaling in Non-Small Cell Lung Cancer Cells.Biomedicines · 2022Article
- FAK in Cancer: From Mechanisms to Therapeutic Strategies.International journal of molecular sciences · 2022Review
- Article
- The Effect of Terpenoid Natural Chinese Medicine Molecular Compound on Lung Cancer Treatment.Evidence-based complementary and alternative medicine : eCAM · 2021Review
- Involvement of the FAK Network in Pathologies Related to Altered Mechanotransduction.International journal of molecular sciences · 2020Review
- Lamin A/C: Function in Normal and Tumor Cells.Cancers · 2020Review
- Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Focal adhesion kinase (FAK) is a non-receptor kinase that facilitates tumor aggressiveness. The effects of FAK inhibition include arresting proliferation, limiting metastasis, and inhibiting angiogenesis. PF-573228 is an ATP-competitive inhibitor of FAK. Treating lung cancer cells with PF-573228 resulted in FAK inactivation and changes in the expressions of lamin A/C and nuclear deformity. Since lamin A/C downregulation or deficiency was associated with cellular senescence, the senescence-associated β-galactosidase (SA-β-gal) assay was used to investigate whether PF-573228 treatment drove cellular senescence, which showed more SA-β-gal-positive cells in culture. p53 is known to play a pivotal role in mediating the progression of cellular senescence, and the PF-573228-treated lung cancer cells resulted in a higher p53 expression level. Subsequently, the FAK depletion in lung cancer cells was employed to confirm the role of FAK inhibition on cellular senescence. FAK depletion and pharmacological inhibition of lung cancer cells elicited similar patterns of cellular senescence, lamin A/C downregulation, and p53 upregulation, implying that FAK signaling is associated with the expression of p53 and the maintenance of lamin A/C levels to shape regular nuclear morphology and manage anti-senescence. Conversely, FAK inactivation led to p53 upregulation, disorganization of the nuclear matrix, and consequently cellular senescence. Our data suggest a new FAK signaling pathway, in that abolishing FAK signaling can activate the senescence program in cells. Triggering cellular senescence could be a new therapeutic approach to limit tumor growth.
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