title: Musca domestica larva lectin induces apoptosis in BEL-7402 cells through a Ca(2+)/JNK-mediated mitochondrial pathway.
abstract: Although Musca domestica larvae lectin (MLL) is able to inhibit cancer cell proliferation and to induce cancer cell apoptosis, the molecular mechanism(s) responsible for these processes remain elusive. In the current study, the signaling network underlying the MLL-induced apoptosis of human hepatoma BEL-7402 cell was investigated. Our data found out that MLL causes a sustained increase of the intracellular Ca(2+) and this process was prevented by the intracellular calcium chelator, BAPTA-AM, suggesting the involvement of intracellular Ca(2+) in MLL-induced cell apoptosis. MLL also causes the production of reactive oxygen species and elevates the phosphorylation status of JNK, processes associated with the increased cytoplasmic Ca(2+). The mitochondrial permeability transition pore (MPTP) opening study showed that MLL treatment of BEL-7402 cells results in the opening of MPTP and a reduction of mitochondrial transmembrane potential. In such condition, cytochrome-c was detected to be released from mitochondria to cytoplasm through the MPTP. This eventually activates caspase-3 and thus results in apoptosis of the tested BEL-7402 cells. According to a comprehensive review of all the evidence, it is concluded that MLL induces apoptosis of BEL-7402 cells through a Ca(2+)/JNK-mediated MPTP pathway.
authors.affiliation: Key Laboratory of Food Nutrition and Safety, Ministry of Education, Tianjin University of Science & Technology, No. 29, 13th Avenue, Tianjin Economy Technological Development Area, Tianjin, 300457, People's Republic of China. wangchunling@tust.edu.cn
authors.forename: Chun-Ling
authors.initials: CL
authors.lastname: Wang
authors.forename: Yan
authors.initials: Y
authors.lastname: Xia
authors.forename: Jian-Zeng
authors.initials: JZ
authors.lastname: Nie
authors.forename: Minghui
authors.initials: M
authors.lastname: Zhou
authors.forename: Rong-Ping
authors.initials: RP
authors.lastname: Zhang
authors.forename: Li-Li
authors.initials: LL
authors.lastname: Niu
authors.forename: Li-Hua
authors.initials: LH
authors.lastname: Hou
authors.forename: Xiao-Hong
authors.initials: XH
authors.lastname: Cao
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects*; D002118:Calcium / Q000378:metabolism*; D053148:Caspase 3 / Q000378:metabolism; D045744:Cell Line, Tumor; D045304:Cytochromes c / Q000378:metabolism; D004533:Egtazic Acid / Q000031:analogs & derivatives / Q000494:pharmacology; D006793:Houseflies / Q000378:metabolism; D006801:Humans; D048031:JNK Mitogen-Activated Protein Kinases / Q000378:metabolism*; D007814:Larva / Q000378:metabolism; D037102:Lectins / Q000494:pharmacology*; D020935:MAP Kinase Signaling System; D053078:Membrane Potential, Mitochondrial / Q000187:drug effects; D008928:Mitochondria / Q000378:metabolism*; D033681:Mitochondrial Membrane Transport Proteins / Q000187:drug effects; D000083162:Mitochondrial Permeability Transition Pore; D010766:Phosphorylation; D017382:Reactive Oxygen Species / Q000378:metabolism
chemical_list: D037102:Lectins; D033681:Mitochondrial Membrane Transport Proteins; D000083162:Mitochondrial Permeability Transition Pore; D017382:Reactive Oxygen Species; C070379:1,2-bis(2-aminophenoxy)ethane N,N,N',N'-tetraacetic acid acetoxymethyl ester; D004533:Egtazic Acid; D045304:Cytochromes c; D048031:JNK Mitogen-Activated Protein Kinases; D053148:Caspase 3; D002118:Calcium