Fengycin inhibits the growth of the human lung cancer cell line 95D through reactive oxygen species production and mitochondria-dependent apoptosis

• DOI: 10.1097/cad.0b013e3283611395
• Publication Date: 2013-04-02T15:39:08Z
• Authors: Hongping Yin; Chuanlong Guo; Ying Wang; Dan Liu; Yunbin Lv; Fengxia Lv; Zhaoxin Lu
• Keywords: 0303 health sciences; Lung Neoplasms; Microscopy, Confocal; L-Lactate Dehydrogenase; Cell Cycle; Cyclin-Dependent Kinase 4; Antineoplastic Agents; Apoptosis; Flow Cytometry; 3. Good health; Gene Expression Regulation, Neoplastic; Lipopeptides; 03 medical and health sciences; Caspases; Cell Line, Tumor; Mitochondrial Membranes; Humans; Calcium; Cyclin D1; Reactive Oxygen Species; Genes, Neoplasm

To investigate the antitumor activity and action mechanism of fengycin using human lung cancer cell line 95D. The was tested in vitro vivo. Reactive oxygen species production, Ca(2+) uptake, mitochondrial membrane potential loss induced by 95D cells were measured flow cytometry a laser confocal microscope. Lactate dehydrogenase release caspase fengycin-treated assayed cytotoxicity detection kits. Apoptosis triggered identified 4,6-diamidino-2-phenylindole (DAPI) staining cytometry. effects on cell-cycle apoptosis-related proteins evaluated quantitative reverse-transcription PCR western blot. Treatment with not only significantly decreased proliferation various lines including but inhibited growth xenografted nude mice. Fengycin also reactive production as well lactate loss. Further experiments showed that could trigger apoptosis cause arrest at G0/G1 stage downregulating cyclin D1 cyclin-dependent kinase 4 (CDK4). While investigating expression proteins, found to induce through pathway, evidenced increased activity, Bax expression, cytochrome c into cytoplasm, Bcl-2 levels. can inhibit regulating cycle promoting apoptosis, suggesting it may have an anticancer treatment.