PURPOSE: Non-small lung cancer (NSLC) is one of the leading causes of cancer-related deaths world over. Excempting operable cases the treatments for NSCLC mainly include chemotherapy and radiotherapy. However, the survival rate for NSCLC is still far from satsifactory. Moreover, chemotherapy has lot of associated side effects. Therefore, there is an urgent need to look for novel and more viable treatment options. Against this background, the present study was designed to evaluate the anticancer activity of α-Bisabolol against NSCLC. METHODS: Cell viability was assessed by MTT assay. Apoptosis was determined by DAPI and annexin V/propidium iodide (PI) staining. Mitochondrial membrane potential (MMP) and cell cycle analysis were determined by flow cytometry. Cell migration was investigated by wound healing assay and protein expression was evaluated by western blotting. RESULTS: α-Bisabolol exerted significant anticancer activity on A549 NSCLC cells with IC50 of 15 μM. The anticancer effects of α-Bisabolol were found to be due to G2/M cell cycle arrest and mitochondrial apoptosis. α-Bisabolol also inhibited cell migration of A549 cells dose-dependently. Moreover, the results showed that α-Bisabolol could inhibit the PI3K/AKT signalling pathway in a dose-dependent manner. The results of the present study indicate that α-Bisabolol exerted selective anticancer effects on A549 cells via induction of cell cycle arrest, mitochondrial apoptosis and inhibition of PI3K/Akt signalling pathways. CONCLUSIONS: This molecule showed promising anticancer features and could be developed as a potent lead candidate for the management and treatment of NSCLC.
PURPOSE:Non-small lung cancer (NSLC) is one of the leading causes of cancer-related deaths world over. Excempting operable cases the treatments for NSCLC mainly include chemotherapy and radiotherapy. However, the survival rate for NSCLC is still far from satsifactory. Moreover, chemotherapy has lot of associated side effects. Therefore, there is an urgent need to look for novel and more viable treatment options. Against this background, the present study was designed to evaluate the anticancer activity of α-Bisabolol against NSCLC. METHODS: Cell viability was assessed by MTT assay. Apoptosis was determined by DAPI and annexin V/propidium iodide (PI) staining. Mitochondrial membrane potential (MMP) and cell cycle analysis were determined by flow cytometry. Cell migration was investigated by wound healing assay and protein expression was evaluated by western blotting. RESULTS: α-Bisabolol exerted significant anticancer activity on A549 NSCLC cells with IC50 of 15 μM. The anticancer effects of α-Bisabolol were found to be due to G2/M cell cycle arrest and mitochondrial apoptosis. α-Bisabolol also inhibited cell migration of A549 cells dose-dependently. Moreover, the results showed that α-Bisabolol could inhibit the PI3K/AKT signalling pathway in a dose-dependent manner. The results of the present study indicate that α-Bisabolol exerted selective anticancer effects on A549 cells via induction of cell cycle arrest, mitochondrial apoptosis and inhibition of PI3K/Akt signalling pathways. CONCLUSIONS: This molecule showed promising anticancer features and could be developed as a potent lead candidate for the management and treatment of NSCLC.