BI-1 enhances Fas-induced cell death through a Na+/H+-associated mechanism
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The role of Bax inhibitor-1 (BI-1) in the protective mechanismagainst apoptotic stimuli has been studied; however, as little isknown about its role in death receptor-mediated cell death,this study was designed to investigate the effect of BI-1 onFas-induced cell death, and the underlying mechanisms. HT1080 adenocarcinoma cells were cultured in highconcentration of glucose media and transfected with vectoralone (Neo cells) or BI-1-vector (BI-1 cells), and treated withFas. In cell viability, apoptosis, and caspase-3 analyses, theBI-1 cells showed enhanced sensitivity to Fas. Fas significantlydecreased cytosolic pH in BI-1 cells, compared with Neo cells,and this decrease correlated with BI-1 oligomerization,mitochondrial Ca2+ accumulation, and significant inhibition ofsodium-hydrogen exchanger (NHE) activity. Compared withNeo cells, a single treatment of BI-1 cells with the NHEinhibitor EIPA or siRNA against NHE significantly increasedcell death, which suggests that the viability of BI-1 cells isaffected by the maintenance of intracellular pH homeostasisthrough NHE.
Abstract
The role of Bax inhibitor-1 (BI-1) in the protective mechanismagainst apoptotic stimuli has been studied; however, as little isknown about its role in death receptor-mediated cell death,this study was designed to investigate the effect of BI-1 onFas-induced cell death, and the underlying mechanisms. HT1080 adenocarcinoma cells were cultured in highconcentration of glucose media and transfected with vectoralone (Neo cells) or BI-1-vector (BI-1 cells), and treated withFas. In cell viability, apoptosis, and caspase-3 analyses, theBI-1 cells showed enhanced sensitivity to Fas. Fas significantlydecreased cytosolic pH in BI-1 cells, compared with Neo cells,and this decrease correlated with BI-1 oligomerization,mitochondrial Ca2+ accumulation, and significant inhibition ofsodium-hydrogen exchanger (NHE) activity. Compared withNeo cells, a single treatment of BI-1 cells with the NHEinhibitor EIPA or siRNA against NHE significantly increasedcell death, which suggests that the viability of BI-1 cells isaffected by the maintenance of intracellular pH homeostasisthrough NHE.
참고문헌 (25)
- Xu, Q., "Bax inhibitor-1, a mammalian apoptosis suppressor identified by functional screening in yeast", Mol. Cell, 1, pp.337~346 (1998)
- Chae, H. J., "BI-1 regulates an apoptosis pathway linked to endoplasmic reticulum stress", Mol. Cell, 15, pp.355~366 (2004)
- Kim, H. R., "Bax Inhibitor-1 Is a pH-dependent regulator of Ca2+ channel activity in the endoplasmic reticulum", J. Biol. Chem, 283, pp.15946~15955 (2008)
- Xiang-yong, L., "Overexpression of Bax inhibitor-1 (BI-1) induces cell transformation in NIH3T3 cells", Cell Biol. Int, 34, pp.1099~1104 (2010)
- Grzmil, M., "Bax inhibitor-1 is overexpressed in prostate cancer and its specific down-regulation by RNA interference leads to cell death in human prostate carcinoma cells", Am. J. Pathol, 163, pp.543~552 (2003)
- Lee, G. H., "BAX inhibitor-1 enhances cancer metastasis by altering glucose metabolism and activating the sodium-hydrogen exchanger: the alteration of mitochondrial function", Oncogene, 29, pp.2130~2141 (2010)
- Liu, Y., "CHP1-Mediated NHE1 Biosynthetic Maturation Is Required for Purkinje Cell Axon Homeostasis", J. Neurosci, 33, pp.12656~12669 (2013)
- Undem, C., "Endothelin-1 augments Na(+)", H(+) exchange activity in murine pulmonary arterial smooth muscle cells via Rho kinase, 2012, pp.7, e46303~
- Lee, G. H., "Enhanced lysosomal activity is involved in Bax inhibitor-1-induced regulation of the endoplasmic reticulum (ER) stress response and cell death against ER stress: involvement of vacuolar H+-ATPase (V-ATPase)", J. Biol. Chem, 286, pp.24743~24753 (2011)
- Wahl, M. L., "Regulation of intracellular pH in human melanoma: potential therapeutic implications", Mol. Cancer Ther, 1, pp.617~628 (2002)
- Boldin, M. P., "Involvement of MACH, a novel MORT1", FADD-interacting protease, in Fas, Cell, pp.1996, 85[DOI]
- Brunner, T., "Fas (CD95", Apo-1) ligand regulation in T cell homeostasis, cell-mediated cytotoxicity and immune pathology, 2003, pp.15, 167~176
- Hannun, Y. A., "Apoptosis and the dilemma of cancer chemotherapy", Blood, 89, pp.1845~1853 (1997)
- Lang, F., "Inhibition of Jurkat-T-lymphocyte Na+", H+-exchanger by CD95(Fas, Pflugers Arch, pp.2000, 440[DOI]
- Warburg, O., "Effect of riboflavin and delta-aminolevulinic acid on growing cancer cells in vitro", Hoppe. Seylers. Z. Physiol. Chem, 348, pp.1683~1685 (1967)
- Wood, T. E., "A novel inhibitor of glucose uptake sensitizes cells to FAS-induced cell death", Mol. Cancer Ther, 7, pp.3546~3555 (2008)
- Lu, J. Y., "Role of Fas and FasL expression in apoptosis of pulmonary artery smooth muscle cells in hypoxia induced by inhibition of Na+", H+ exchanger isoform- 1 in rat, 2005, pp.17, 515~518
- Di Sario, A., "Selective inhibition of ion transport mechanisms regulating intracellular pH reduces proliferation and induces apoptosis in cholangiocarcinoma cells", Dig. Liver Dis, 39, pp.60~69 (2007)
- Thangaraju, M., "Interdependent regulation of intracellular acidification and SHP-1 in apoptosis", Cancer Res, 59, pp.1649~1654 (1999)
- Luo, J., "Inhibition of the regulation of intracellular pH: potential of 5-(N,N-hexamethylene) amiloride in tumour-selective therapy", Br. J. Cancer, 70, pp.617~624 (1994)
- Kennedy, K. M., "Tumor metabolism of lactate: the influence and therapeutic potential for MCT and CD147 regulation", Future. Oncol, 6, pp.127~148 (2010)
- Fang, J., "The H+-linked monocarboxylate transporter (MCT1", SLC16A1): a potential therapeutic target for high-risk neuroblastoma, 2006, pp.70, 2108~2115
- Grzmil, M., "Expression and functional analysis of Bax inhibitor- 1 in human breast cancer cells", J. Pathol, 208, pp.340~349 (2006)
- Schmits, R., "Analysis of the antibody repertoire of astrocytoma patients against antigens expressed by gliomas", Int. J. Cancer, 98, pp.73~77 (2002)
- Sano, R., "Endoplasmic reticulum protein BI-1 regulates Ca(2)(+)-mediated bioenergetics to promote autophagy", Genes Dev, 26, pp.1041~1054 (2012)