Growth Inhibition and Cell Death Induction by Resveratrol in Human Lung Adenocarcinoma Cells
Ming‐Huan Chan, Kuei-Ping Chen
Abstract
Ming‐Huan Chan, Kuei-Ping Chen
Abstract
This study investigated the effects of resveratrol on cell growth in human lung adenocarcinoma A549 cells and normal swine tracheal epithelial cells (STECs), and compared their cytotoxic responses. Materials and Methods: Cell viability and cell growth were measured by trypan blue dye exclusion and MTT reduction assay. The intracellular Ca(superscript 2+) levels were determined by fluorescent imaging. Protein expression in apoptotic signaling was measured by Western blotting. Results: Data showed that resveratrol not only induced cell death but also inhibited cell growth in a concentration- and time-dependent manner. Importantly, resveratrol was less toxic to STECs than to lung adenocarcinoma, indicating that adenocarcinoma is largely sensitive to resveratrol. Furthermore, cell death was consistent with the apoptotic signals triggered by resveratrol, with an increase in cytosolic Ca(superscript 2+) levels and a marked increase in the expression of p53 and Bax proteins. Conclusion: Resveratrol may have potential for prevention and treatment of lung adenocarcinoma; normal airway epithelia were more resistance than lung adenocarcinoma to the cytotoxicity of resveratrol.
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This study investigated the effects of resveratrol on cell growth in human lung adenocarcinoma A549 cells and normal swine tracheal epithelial cells (STECs), and compared their cytotoxic responses. Materials and Methods: Cell viability and cell growth were measured by trypan blue dye exclusion and MTT reduction assay. The intracellular Ca(superscript 2+) levels were determined by fluorescent imaging. Protein expression in apoptotic signaling was measured by Western blotting. Results: Data showed that resveratrol not only induced cell death but also inhibited cell growth in a concentration- and time-dependent manner. Importantly, resveratrol was less toxic to STECs than to lung adenocarcinoma, indicating that adenocarcinoma is largely sensitive to resveratrol. Furthermore, cell death was consistent with the apoptotic signals triggered by resveratrol, with an increase in cytosolic Ca(superscript 2+) levels and a marked increase in the expression of p53 and Bax proteins. Conclusion: Resveratrol may have potential for prevention and treatment of lung adenocarcinoma; normal airway epithelia were more resistance than lung adenocarcinoma to the cytotoxicity of resveratrol.
Key concepts: Resveratrol, Viability assay, Apoptosis, Adenocarcinoma, Programmed cell death, Trypan blue, Cytotoxicity, Cell growth