Restoration of p53/miR-34a regulatory axis decreases survival advantage and ensures Bax-dependent apoptosis of non-small cell lung carcinoma cells

被引：102

作者：

Chakraborty, Samik ^{[1
]}

Mazumdar, Minakshi ^{[1
]}

Mukherjee, Shravanti ^{[1
]}

Bhattacharjee, Pushpak ^{[1
]}

Adhikary, Arghya ^{[1
]}

Manna, Argha ^{[1
]}

Chakraborty, Sreeparna ^{[1
]}

Khan, Poulami ^{[1
]}

Sen, Aparna ^{[2
]}

Das, Tanya ^{[1
]}

机构：

[1] Bose Inst, Div Mol Med, Kolkata 700054, W Bengal, India

[2] Lady Brabourne Coll, Kolkata, India

来源：

FEBS LETTERS | 2014年 / 588卷 / 04期

关键词：

Apoptosis; Bcl-2 associated X protein; B cell lymphoma-2; Capsaicin; DNA-damage; MiR-34a; Mitochondrial transmembrane potential; p53; Reactive oxygen species; POSTTRANSLATIONAL MODIFICATIONS; MOLECULAR-MECHANISMS; PROGNOSTIC MARKER; OXIDATIVE STRESS; DOWN-REGULATION; P53; CAPSAICIN; MIR-34A; CANCER; PHOSPHORYLATION;

D O I：

10.1016/j.febslet.2013.11.040

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

070307 [化学生物学]; 071010 [生物化学与分子生物学];

摘要：

Tumor-suppressive miR-34a, a direct target of p53, has been shown to target several molecules of cell survival pathways. Here, we show that capsaicin-induced oxidative DNA damage culminates in p53 activation to up-regulate expression of miR-34a in non-small cell lung carcinoma (NSCLC) cells. Functional analyses further indicate that restoration of miR-34a inhibits B cell lymphoma-2 (Bcl-2) protein expression to withdraw the survival advantage of these resistant NSCLC cells. In such a proapoptotic cellular milieu, where drug resistance proteins are also down-regulated, p53-trans-activated Bcl-2 associated X protein (Bax) induces apoptosis via the mitochondrial death cascade. Our results suggest that p53/miR-34a regulatory axis might be critical in sensitizing drug-resistant NSCLC cells. (C) 2014 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.

引用

收藏

页码：549 / 559

页数：11

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