p110 and p110 isoforms of PI3K are involved in protection against H2O2 induced oxidative stress in cancer cells

被引:1
作者
Singh, Paramjeet [1 ,2 ]
Bano, Nasima [1 ,2 ]
Hossain, Md Mehedi [1 ,2 ]
Basit, Rafia [1 ,2 ]
Dar, Mohd Jamal [1 ,2 ]
机构
[1] Acad Sci & Innovat Res, New Delhi, India
[2] Indian Inst Integrat Med, CSIR, Canc Pharmacol Div, Jammu 180001, J&K, India
关键词
PI3K signalling; Akt; Apoptosis; Breast cancer; PROTEIN-KINASE B; PIK3CA GENE; PATHWAY; APOPTOSIS; MUTATIONS; OVARIAN; AKT; P110-ALPHA; ACTIVATION; SURVIVAL;
D O I
10.1007/s12282-018-0933-x
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
PurposePhosphatidylinositol-3 kinases (PI3Ks) are involved in regulating cell growth, proliferation, differentiation, apoptosis and survival. p110 and p110, two ubiquitously expressed isoforms of PI3K signalling, are involved in growth factor mediated signaling and survival by generating second messengers. Earlier, we have generated GFP-fusion proteins of p110 and p110 and expressed them in normal and cancer cell-lines to investigate their subcellular localization and their role in various activities. Here, we sought to examine the role of p110 and p110 isoforms in protecting MCF-7 breast cancer cells against oxidative stress.Material methodsWe performed cytotoxicity assays, DNA transfection, Plasmid DNA preparation, western blotting, flourscence microscopy and statistical analysis.ResultsTo know whether p110 and p110 are involved in protecting MCF-7 breast cancer cells against oxidative stress, we subjected MCF-7 cells to H2O2 treatment and observed a dose dependent decrease in cell viability and a marked increase in the levels of pro-apoptotic markers which include PARP, Bcl-2, Bax and procaspase-9. We then over-expressed recombinant GFP-fusion p110 and p110 proteins in MCF-7 cells and observed a significant decrease in apoptosis and a concomitant increase in pAkt levels.ConclusionWe report the involvement of p110 and p110 isoforms of Class 1A PI3K signalling in rescue from oxidative stress-induced apoptosis in MCF-7 cells in Akt dependent manner.
引用
收藏
页码:378 / 385
页数:8
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