Anticancer Potential of Flaxseed Extract Against Human Lung Cancer Cells (A-549): In Vitro Cytotoxicity, Gene Expression, and Molecular Docking Analysis
DOI:
https://doi.org/10.63682/jns.v14i21S.5612Keywords:
Wound healing assay 1, Molecular docking, Gamma-tocopherol, Apoptosis, A-549 cells, Lung cancer, Flaxseed extractAbstract
Background: Lung cancer remains a leading cause of cancer-related mortality globally. Natural compounds derived from plants, such as flaxseed extract, are increasingly explored for their anticancer properties due to their bioactive phytochemicals
Objective: To investigate the cytotoxic and apoptotic effects of flaxseed extract on human lung cancer cells (A-549), including its influence on gene expression, cell migration, and interaction with tumor suppressor protein P53 via molecular docking.
Methods: A-549 cells were treated with flaxseed extract at varying concentrations (20 and 40 μg/mL) for 24 h. Cytotoxicity was assessed using the MTT assay. Cell morphology and apoptosis were examined via phase-contrast microscopy and DAPI staining. RT-PCR was performed to analyze the expression of apoptosis-related genes. Molecular docking was conducted using gamma-tocopherol (from flaxseed) with P53 protein (PDB ID: 2AHI). A scratch wound healing assay was carried out to evaluate cell migration.
Results: MTT assay revealed significant dose-dependent cytotoxicity (p < 0.05). Morphological analysis showed reduced cell numbers, shrinkage, and membrane blebbing. DAPI staining confirmed nuclear condensation, indicating apoptosis. RT-PCR analysis showed modulation of apoptosis-related genes. Molecular docking revealed a binding energy of -6.7 kcal/mol between gamma-tocopherol and P53, suggesting a stable interaction. The wound healing assay showed inhibited cell migration at 40 μg/mL, indicating anti-metastatic potential.
Conclusion: Flaxseed extract demonstrates strong anticancer activity against A-549 lung cancer cells through induction of apoptosis, modulation of gene expression, and inhibition of cell migration. Gamma-tocopherol may enhance the tumor-suppressive activity of P53, supporting its potential as a therapeutic agent.
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