OBJECTIVE: To investigate the apoptosis-inducing effect of cantharidin in human lung cancer cells A549 and its molecular mechanisms. METHODS: MTT assay was used to determine A549 cells proliferation. Light and electron microscopy, FACScan, Annexin V-FITC staining and DNA gel electrophoresis were used to detect apoptosis. The expression of bcl-2, Bax and survivin were examined by Western blot. RESULTS: Cantharidin inhibited the proliferation of A549 cells. The cells treated with cantharidin showed a typical apoptotic morphology and hypodiploid peak before G(1) phase. Flow cytometry analysis with annexin quantitatively further confirmed the increase of cell apoptosis. DNA of treated A549 cells depicted a ladder pattern characteristic of apoptosis, indicating the presence of DNA fragmentation. Western blot assay showed that cantharidin increased the level of Bax expression and inhibited the level of bcl-2 and survivin expression. CONCLUSION: Cantharidin can induce A549 cells apoptosis mainly via regulation of Bax, bcl-2 and survivin expression.
OBJECTIVE: To investigate the apoptosis-inducing effect of cantharidin in humanlung cancer cells A549 and its molecular mechanisms. METHODS:MTT assay was used to determine A549 cells proliferation. Light and electron microscopy, FACScan, Annexin V-FITC staining and DNA gel electrophoresis were used to detect apoptosis. The expression of bcl-2, Bax and survivin were examined by Western blot. RESULTS:Cantharidin inhibited the proliferation of A549 cells. The cells treated with cantharidin showed a typical apoptotic morphology and hypodiploid peak before G(1) phase. Flow cytometry analysis with annexin quantitatively further confirmed the increase of cell apoptosis. DNA of treated A549 cells depicted a ladder pattern characteristic of apoptosis, indicating the presence of DNA fragmentation. Western blot assay showed that cantharidin increased the level of Bax expression and inhibited the level of bcl-2 and survivin expression. CONCLUSION:Cantharidin can induce A549 cells apoptosis mainly via regulation of Bax, bcl-2 and survivin expression.
Authors: Kathy Bonness; Ileana V Aragon; Beth Rutland; Solomon Ofori-Acquah; Nicholas M Dean; Richard E Honkanen Journal: Mol Cancer Ther Date: 2006-11 Impact factor: 6.261