Vol.5 No.3 – 3 :Curcumin suppresses cellular adhesion and migration of A549 lung cancer cells via a LIMK1/MLCK dependent mechanism
By: Ahmed A. Soffar 1, Cecil A. Matta 2, Saleh O. Albatati 3
1. Division of Molecular Biology, Department of Zoology, Faculty of Science, Alexandria University, Alexandria, Egypt.
2. Department of Zoology, Faculty of Science, Alexandria University, Alexandria, Egypt.
3. Basic Medical Sciences Department, College of Medicine, Mukalla-B.O: (50512-50511), Hadhramaut, Yemen.
Abstract
Cancer cell migration is a major cause of mortality in lung cancer patients. Despite intensive research regarding its efficacy in cancer treatment, the anti-metastatic properties of curcumin have been poorly investigated. Therefore, this work aims to explore the potential anti-migratory and anti-adhesive properties of curcumin on lung cancer cells. We also investigated the underlying molecular mode of action of curcumin. We performed scratch and adhesion assays to investigate the migratory and adhesive potentials of A549 cells. The cellular topological differences upon curcumin treatment were investigated using Scanning Electron Microscope. We also investigated the molecular mechanism triggered by curcumin using quantitative real-time PCR. In addition, we performed MTT toxicity assay to explore the toxic potential of curcumin on cancer cells. Student’s t-test was applied for evaluating the data significance using Microsoft Excel 2016. Our results showed that curcumin attenuates migration and adhesion of A549 cancer cells at non-toxic concentrations. In coincidence, the scanning electron microscope study showed a decreased density of lamellipodia and filopodia upon curcumin treatment. Interestingly, we found that the expression levels of LIMK1 and MLCK genes were downregulated upon curcumin application. Taken together, curcumin inhibits the migration and adhesion abilities of lung cancer cells and could possibly be used as a therapeutic agent against cancer cell migration. The underlying mechanism involves modulation of the expression levels of critical molecular targets including LIMK1 and MLCK proteins.
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