Glucose starvation-induced oxidative stress causes mitochondrial dysfunction and apoptosis via Prohibitin 1 upregulation in human breast cancer cells

被引:48
作者
Raut, Ganesh Kumar [1 ,2 ]
Chakrabarti, Moumita [1 ,2 ]
Pamarthy, Deepika [1 ,2 ]
Bhadra, Manika Pal [1 ,2 ]
机构
[1] CSIR Indian Inst Chem Technol, Dept Appl Biol, Uppal Rd, Hyderabad 500007, Telangana, India
[2] Acad Sci & Innovat Res AcSIR, Training & Dev Complex,CSIR Campus,CSIR Rd, Chennai 600113, Tamil Nadu, India
关键词
Apoptosis; Dynamin-related protein 1 (DRP1); Glucose starvation (GS); Oxidative stress; Prohibitin 1 (PHB1); REACTIVE OXYGEN; POTENTIAL BIOMARKER; FLUORESCENT-PROBES; FAMILY-MEMBERS; PROLIFERATION; FISSION; METABOLISM; CARCINOMA; ROLES; CRISTAE;
D O I
10.1016/j.freeradbiomed.2019.09.020
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
In recent years there has been an upsurge in research focusing on reprogramming cancer cells through understanding of their metabolic signatures. Alterations in mitochondrial bioenergetics and impaired mitochondrial function may serve as effective targeting strategies especially in triple-negative breast cancers (TNBCs) where hormone receptors and endocrine therapy are absent. Glucose starvation (GS) of MDA-MB-231 and MCF-7 breast cancer cells showed decrease in mitochondrial Oxygen Consumption Rate (OCR), which was rescuable to control level through addition of exogenous antioxidant N-Acetyl Cysteine (NAC). Mechanistically, GS led to increase in mitochondrial ROS and upregulation of the pleiotropic protein, Prohibitin 1 (PHB1), leading to its dissociation from Dynamin-related protein 1 (DRP1), perturbance of mitochondrial membrane potential (MMP) and triggering of the apoptosis cascade. PHB1 also reduced the invasive and migratory potential of both cell lines. We emphasize that glucose starvation remarkably sensitized the highly glycolytic metastatic TNBC cell line, MDAMB-231 to apoptosis and decreased its migratory potential. Based on our findings, additional TNBC cell lines can be evaluated and a nutritional paradigm be proposed for anticancer therapy.
引用
收藏
页码:428 / 441
页数:14
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