Buforin IIb induces endoplasmic reticulum stress-mediated apoptosis in HeLa cells |
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| Affiliation: | 1. University of North Carolina Lineberger Comprehensive Cancer Center, Advanced Cellular Therapeutics Facility, Chapel Hill, North Carolina, USA. ISCT North America, Past Regional Vice President 2012–2014;2. Moffitt Cancer Center and Research Institute, Tampa, Florida, USA. Chair, ISCT NA LRA Committee, 2014–2016 and Co-Editor of the Telegraft;3. St Jude Children''s Research Hospital, Memphis, Tennessee, USA. ISCT Past Co-Chair, NA LRA Committee 2011–2014. ISCT North America, Regional Vice President 2014–2016;4. Division of Hematology, Cell Therapy Laboratory, The Ohio State University, Columbus, Ohio, USA. ISCT Global Secretary, 2013–2016 and Editor in Chief of Telegraft;1. Division of Hematology, Cell Therapy Laboratory, The Ohio State University, Columbus, Ohio, USA, International Society for Cellular Therapy (ISCT) Global Secretary 2013–2016, Editor in Chief of Telegraft;2. University of Minnesota Center for Bioethics and School of Public Health, Minneapolis, Minnesota, USA, Member at Large of the ISCT Presidential Task Force on the Use of Unproven Cellular Therapies;3. School of Public Policy, Georgia Institute of Technology, Atlanta, Georgia, USA, Member at large of the ISCT Presidential Task Force on the Use of Unproven Cellular Therapies |
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| Abstract: | ![]()
Buforin IIb, a novel cell-penetrating anticancer peptide derived from histone H2A, has been reported to induce mitochondria-dependent apoptosis in tumor cells. However, increasing evidence suggests that endoplasmic reticulum and mitochondria cooperate to signal cell death. In this study, we investigated the mechanism of buforin IIb-induced apoptosis in human cervical carcinoma HeLa cells by focusing on ER stress-mediated mitochondrial membrane permeabilization. Two-dimensional PAGE coupled with MALDI-TOF and western blot analysis showed that buforin IIb treatment of HeLa cells resulted in upregulation of ER stress proteins. PBA (ER stress inhibitor) and BAPTA/AM (Ca2+ chelator) pretreatment rescued viability of buforin IIb-treated cells through abolishing phosphorylation of SAPK/JNK and p38 MAPK. SP600125 (SAPK/JNK inhibitor) and SB203580 (p38 MAPK inhibitor) attenuated down-regulation of Bcl-xL/Bcl-2, mitochondrial translocation of Bax, and cytochrome c release from mitochondria. Taken together, our data suggest that the ER stress pathway has an important role in the buforin IIb-induced apoptosis in HeLa cells. |
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| Keywords: | Buforin IIb Anticancer peptide Apotosis ER stress Mitochondrial membrane permeabilization AMP" },{" #name" :" keyword" ," $" :{" id" :" kw0035" }," $$" :[{" #name" :" text" ," _" :" antimicrobial peptide ER" },{" #name" :" keyword" ," $" :{" id" :" kw0045" }," $$" :[{" #name" :" text" ," _" :" endoplasmic reticulum SAPK/JNK" },{" #name" :" keyword" ," $" :{" id" :" kw0055" }," $$" :[{" #name" :" text" ," _" :" stress-activated protein kinase/Jun-amino-terminal kinase p38 MAPK" },{" #name" :" keyword" ," $" :{" id" :" kw0065" }," $$" :[{" #name" :" text" ," _" :" p38 mitogen-activated protein kinase CHOP" },{" #name" :" keyword" ," $" :{" id" :" kw0075" }," $$" :[{" #name" :" text" ," _" :" C/EBP homologous protein GRP78" },{" #name" :" keyword" ," $" :{" id" :" kw0085" }," $$" :[{" #name" :" text" ," $$" :[{" #name" :" __text__" ," _" :" 78" },{" #name" :" hsp" ," $" :{" sp" :" 0.25" }},{" #name" :" __text__" ," _" :" kDa glucose-regulated protein Bcl-2" },{" #name" :" keyword" ," $" :{" id" :" kw0095" }," $$" :[{" #name" :" text" ," _" :" B cell lymphoma 2 Bcl-xL" },{" #name" :" keyword" ," $" :{" id" :" kw0105" }," $$" :[{" #name" :" text" ," _" :" B-cell lymphoma-extra large Bax" },{" #name" :" keyword" ," $" :{" id" :" kw0115" }," $$" :[{" #name" :" text" ," _" :" Bcl-2-associated X protein PBA" },{" #name" :" keyword" ," $" :{" id" :" kw0125" }," $$" :[{" #name" :" text" ," _" :" 4-phenylbutyric acid BAPTA/AM" },{" #name" :" keyword" ," $" :{" id" :" kw0135" }," $$" :[{" #name" :" text" ," $$" :[{" #name" :" __text__" ," _" :" 1,2-bis(" },{" #name" :" italic" ," _" :" o" },{" #name" :" __text__" ," _" :" -amimophenoxy)ethane-" },{" #name" :" italic" ," _" :" N" },{" #name" :" __text__" ," _" :" ," },{" #name" :" italic" ," _" :" N" },{" #name" :" __text__" ," _" :" ," },{" #name" :" italic" ," _" :" N" },{" #name" :" __text__" ," _" :" ′," },{" #name" :" italic" ," _" :" N" },{" #name" :" __text__" ," _" :" ′-tetraacetic acid |
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