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Resveratrol Regulates Colorectal Cancer Cell Invasion by Modulation of Focal Adhesion Molecules
Constanze Buhrmann1, Parviz Shayan2,3, Ajay Goel4
1Musculoskeletal Research Group and Tumour Biology, Chair of Vegetative Anatomy, Institute of Anatomy, Faculty of Medicine, LMU Munich, Pettenkoferstrasse 11, D-80336 Munich, Germany. constanze.buhrmann@med.uni-muenchen.de.
Abstract:
Resveratrol, a safe and multi-targeted agent, has been associated with suppression of survival, proliferation and metastasis of cancer, however, the underlying mechanisms for its anti-cancer activity, particularly on cellular signaling during cancer cell migration still remain poorly understood. We investigated the invasion response of two human colorectal cancer (CRC) cells (HCT116 and SW480) to resveratrol and studied the effect of specific pharmacological inhibitors, cytochalasin D (CytD) and focal adhesion kinase-inhibitor (FAK-I) on FAK, cell viability and migration in CRC. We found that resveratrol altered cell phenotype of both CRC cells, reduced cell viability and the results were comparable to FAK-I and CytD. These effects of resveratrol were associated with marked Sirt1 up-regulation, FAK down-regulation, inhibition of focal adhesion and potentiation of effects by combinatorial treatment of resveratrol and inhibitors. Interestingly, inhibition of FAK with FAK-I or treatment with CytD suppressed resveratrol-induced Sirt1 up-regulation and markedly down-regulated FAK expression. Resveratrol or combination treatment with inhibitors significantly activated caspase-3 and potentiated apoptosis. Moreover, resveratrol suppressed invasion and colony forming capacity, cell proliferation, β1-Integrin expression and activation of FAK of cells in alginate tumor microenvironment, similar to FAK-I or CytD. Finally, we demonstrated that resveratrol, FAK-I or CytD inhibited activation of NF-κB, suppressed NF-κB-dependent gene end-products involved in invasion, metastasis, and apoptosis; and these effects of resveratrol were potentiated by combination treatment with FAK-I or CytD. Our data illustrated that the anti-invasion effect of resveratrol by inhibition of FAK activity has a potential beneficial role in disease prevention and therapeutic management of CRC.
Insights
Resveratrol suppresses colorectal cancer (CRC) cell invasion by inhibiting focal adhesion kinase (FAK) signaling. This natural compound shows promise for CRC prevention and therapy, potentially enhancing existing treatments.
Area of Science:
- Oncology
- Molecular Biology
- Pharmacology
Background:
- Resveratrol exhibits anti-cancer properties, but its precise mechanisms in colorectal cancer (CRC) cell migration are unclear.
- Understanding resveratrol's effects on cellular signaling pathways is crucial for its therapeutic application.
Purpose of the Study:
- To investigate resveratrol's impact on CRC cell invasion and underlying molecular mechanisms.
- To evaluate the effects of resveratrol, cytochalasin D (CytD), and focal adhesion kinase inhibitor (FAK-I) on CRC cell behavior and signaling.
Main Methods:
- Assessed resveratrol's effects on HCT116 and SW480 CRC cells, alone and in combination with CytD and FAK-I.
- Analyzed cell viability, phenotype, Sirt1 expression, FAK activation, focal adhesion, caspase-3 activity, β1-Integrin expression, and NF-κB activation.
Main Results:
- Resveratrol reduced CRC cell viability and invasion, comparable to FAK-I and CytD.
- Resveratrol up-regulated Sirt1 and down-regulated FAK, inhibiting focal adhesion.
- Combined treatment with resveratrol and inhibitors potentiated anti-cancer effects, including apoptosis induction and NF-κB inhibition.
Conclusions:
- Resveratrol inhibits CRC cell invasion by targeting FAK activity, offering potential benefits for disease prevention and treatment.
- Resveratrol's synergistic effects with FAK-I and CytD highlight its therapeutic potential in CRC management.
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