PMID- 23247835
OWN - NLM
STAT- MEDLINE
DCOM- 20131209
LR  - 20201209
IS  - 1559-0283 (Electronic)
IS  - 1085-9195 (Linking)
VI  - 66
IP  - 2
DP  - 2013 Jun
TI  - Musca domestica larva lectin induces apoptosis in BEL-7402 cells through a 
      Ca(2+)/JNK-mediated mitochondrial pathway.
PG  - 319-29
LID - 10.1007/s12013-012-9489-0 [doi]
AB  - 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.
FAU - Wang, Chun-Ling
AU  - Wang CL
AD  - 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
FAU - Xia, Yan
AU  - Xia Y
FAU - Nie, Jian-Zeng
AU  - Nie JZ
FAU - Zhou, Minghui
AU  - Zhou M
FAU - Zhang, Rong-Ping
AU  - Zhang RP
FAU - Niu, Li-Li
AU  - Niu LL
FAU - Hou, Li-Hua
AU  - Hou LH
FAU - Cao, Xiao-Hong
AU  - Cao XH
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Cell Biochem Biophys
JT  - Cell biochemistry and biophysics
JID - 9701934
RN  - 0 (Lectins)
RN  - 0 (Mitochondrial Membrane Transport Proteins)
RN  - 0 (Mitochondrial Permeability Transition Pore)
RN  - 0 (Reactive Oxygen Species)
RN  - 139890-68-9 (1,2-bis(2-aminophenoxy)ethane N,N,N',N'-tetraacetic acid 
      acetoxymethyl ester)
RN  - 526U7A2651 (Egtazic Acid)
RN  - 9007-43-6 (Cytochromes c)
RN  - EC 2.7.11.24 (JNK Mitogen-Activated Protein Kinases)
RN  - EC 3.4.22.- (Caspase 3)
RN  - SY7Q814VUP (Calcium)
SB  - IM
MH  - Animals
MH  - Apoptosis/*drug effects
MH  - Calcium/*metabolism
MH  - Caspase 3/metabolism
MH  - Cell Line, Tumor
MH  - Cytochromes c/metabolism
MH  - Egtazic Acid/analogs & derivatives/pharmacology
MH  - Houseflies/metabolism
MH  - Humans
MH  - JNK Mitogen-Activated Protein Kinases/*metabolism
MH  - Larva/metabolism
MH  - Lectins/*pharmacology
MH  - MAP Kinase Signaling System
MH  - Membrane Potential, Mitochondrial/drug effects
MH  - Mitochondria/*metabolism
MH  - Mitochondrial Membrane Transport Proteins/drug effects
MH  - Mitochondrial Permeability Transition Pore
MH  - Phosphorylation
MH  - Reactive Oxygen Species/metabolism
EDAT- 2012/12/19 06:00
MHDA- 2013/12/16 06:00
CRDT- 2012/12/19 06:00
PHST- 2012/12/19 06:00 [entrez]
PHST- 2012/12/19 06:00 [pubmed]
PHST- 2013/12/16 06:00 [medline]
AID - 10.1007/s12013-012-9489-0 [doi]
PST - ppublish
SO  - Cell Biochem Biophys. 2013 Jun;66(2):319-29. doi: 10.1007/s12013-012-9489-0.