Gene interactions and pathways from curated databases and text-mining

◀ Back to BCL2

BCL2 — MMP9

Text-mined interactions from Literome

Vieira et al., Oncogene 2002 : When added to isolated mitochondria, BaxBH3 and Bcl2BH3 induced MMP , which was inhibited by CsA ... In purified mitochondria, two ligands of ANT, bongkrekic acid and the protein vMIA from cytomegalovirus, failed to prevent MMP induced by BaxBH3 or Bcl2BH3 ... BaxBH3Ant and Bcl2BH3Ant caused a mitochondrial membrane permeabilization ( MMP ) and apoptosis, via a mechanism that was not inhibited by overexpressed Bcl-2 or Bcl-X ( L ), yet partially inhibited by cyclosporin A ( CsA ), an inhibitor of the mitochondrial permeability transition pore ... In conclusion, BaxBH3 and Bcl2BH3 induce MMP and apoptosis through a mechanism which overcomes cytoprotection by Bcl-2 and Bcl-X ( L )
Noujaim et al., Oncogene 2002 (Neoplasm Invasiveness...) : This study investigates the effect of N-Myc and Bcl-2 on MMP expression and activation
Wick et al., J Neurochem 2004 (Glioma...) : Both a pseudosubstrate furin inhibitor, decanoyl-Arg-Val-Lys-Arg-chloromethylketone ( dec-RVKR-cmk ), or alpha 1-anti-trypsin Portland ( PDX ), a recombinant furin-inhibitory protein, suppress constitutive and BCL-2 mediated MMP activity and invasion
Shen et al., Biochem Biophys Res Commun 2006 : Moreover, MMP-2 inhibition reduced Bax expression and caspase3 activity, as well as increasing Bcl2 expression
Kim et al., Int J Cancer 2008 (Carcinoma, Squamous Cell...) : Overexpression of Bcl-2 in HN4 cells prevented loss of MMP , nuclear translocation of EndoG and protected cells from the delayed apoptosis induced by cisplatin in the presence of z-VAD-fmk
Zuo et al., Mol Cancer Res 2010 (Carcinoma, Squamous Cell...) : siRNA mediated suppression of N-cadherin expression not only prevented the enhanced invasion but also blocked the increased MMP-9 expression induced by elevated Bcl-2 expression ... Furthermore, the Bcl-2 mediated increase in MMP-9 expression and tumor cell invasion was dependent on fibroblast growth factor receptor-1 or extracellular signal regulated kinase signaling
Zeng et al., J Ethnopharmacol 2010 : Moreover, MWG extract decreased the level of intracellular reactive oxygen species ( ROS ), increased MMP , regulated Bcl-2 family protein expression ( Bcl-2 and Bcl-XL ) and inhibited the release of cytochrome c from the mitochondria
Zhang et al., Curr Mol Med 2012 (Breast Neoplasms...) : Addition of sera obtained from patients treated with combination of radiotherapy and EGCG feeding for 2-8 weeks to in vitro cultures of highly-metastatic human MDA-MB-231 breast cancer cells resulted in the following significant changes : ( 1 ) suppression of cell proliferation and invasion ; ( 2 ) arrest of cell cycles at the G0/G1 phase ; ( 3 ) reduction of activation of MMP9/MMP2 , expressions of Bcl-2/Bax , c-Met receptor, NF-?B, and the phosphorylation of Akt
Lecoeur et al., Cell death & disease 2012 : Pharmacologic inhibitors of the permeability transition pore, Bax/Bak inhibitors, and recombinant Bcl-2 and Bcl-XL proteins do not reduce Tat induced MMP
Rincheval et al., Cell Biol Toxicol 2012 : Second, we have highlighted that during etoposide or TNF-a treatments, intracellular ROS level, MMP and cell death are all regulated by caspases and Bcl-2 , with caspases acting early in the process
Arbab et al., Evidence-based complementary and alternative medicine : eCAM 2012 : We found that dentatin mediated accumulation of reactive oxygen species ( ROS ) and downregulated expression levels of antiapoptotic molecules ( Bcl-2, Bcl-xL , and Survivin ), leading to disruption of mitochondrial membrane potential ( MMP ) , cell membrane permeability, and release of cytochrome c from the mitochondria into the cytosol
Looi et al., PloS one 2013 (Breast Neoplasms) : Increased of reactive oxygen species ( ROS ) production, coupled with downregulation of anti-apoptotic molecules ( Bcl-2 , Bcl-xL ) led to reduction of mitochondrial membrane potential ( MMP ) and release of cytochrome c in both human breast cancer cells treated with vernodalin