The mitochondrial effects of embelin are independent of its MAP kinase regulation: Role of p53 in conferring selectivity towards cancer cells

被引:4
作者
Avisetti, Deepa R. [1 ,2 ,3 ]
Amireddy, Niharika [1 ,2 ,3 ]
Kalivendi, Shasi V. [1 ,2 ,3 ]
机构
[1] Indian Inst Chem Technol, CSIR, Dept Appl Biol, Biochem Lab, Uppal Rd, Hyderabad 500007, TS, India
[2] Indian Inst Chem Technol, CSIR, Acad Sci & Innovat Res AcSIR, Uppal Rd, Hyderabad 500007, TS, India
[3] Queen Mary Univ London, Ctr Clin & Diagnost Oral Sci, London, England
关键词
Embelin; Mitochondrial respiration; Oxidative stress; p38 MAP kinase; p53; Apoptosis; NUCLEAR-FACTOR; APOPTOSIS; INHIBITION; PHOSPHORYLATION; LYMPHOCYTES; SUPPRESSION; PROTEIN;
D O I
10.1016/j.mito.2018.04.007
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Amongst various therapeutic properties of the natural product embelin, its anti-cancer effects are being extensively studied. We observed that, embelin induced apoptosis in A549 cells lacking functional mitochondria (rho 0 cells) indicating that its mitochondrial effects are not primarily responsible for its anti-cancer activity. However, p38 mediated activation of p53 was found to play a pivotal role in governing the apoptotic activity of embelin due to the following observations: a time-dependent activation of p53 and apoptosis by embelin; selective inhibition of p38 inhibited embelin-induced p53 levels. Overall, therapeutic strategies involving embelin and activators of p38 MAP kinase may improve the selective targeting of cancer cells.
引用
收藏
页码:158 / 163
页数:6
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