Curcumin induces the mitochondrial permeability transition pore mediated by membrane protein thiol oxidation

Morin, Didier; Barthelemy, Sophie; Zini, Roland; Labidalle, Serge; Tillement, Jean‐Paul

doi:10.1016/s0014-5793(01)02376-6

Cited by 151 publications

(72 citation statements)

References 42 publications

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“…Therefore, the order of appearance of these signaling events in the figure does not necessarily indicate the actual sequence of cause-effect events in the apoptotic signaling induced by dria in ET-743-treated cells, 4 suggesting that JNK activation could occur downstream of mitochondrial cytochrome c release. This is in agreement with recent reports indicating that curcumin, an agent that has been reported to exert both pro-or anti-apoptotic actions (47)(48)(49)(50)(51)(52)(53)(54), potentiates mitochondrial cytochrome c release (49,53) and can even induce opening of the mitochondrial permeability transition pore (55). Nevertheless, curcumin, a dietary yellow pigment from Curcuma longa, has been reported to affect a great variety of signaling processes in different systems (47)(48)(49)(50)(51)(52)(53)(54), and these pleiotropic effects preclude to reach a clear picture of the hierarchical events occurring in curcumin-pretreated cells.…”

Section: Discussionsupporting

confidence: 93%

Differential Cytostatic and Apoptotic Effects of Ecteinascidin-743 in Cancer Cells

Gajate

Mollinedo

2002

Journal of Biological Chemistry

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We have found that ecteinascidin-743 (ET-743) inhibited cell proliferation at 1-10 ng/ml, leading to S and G 2 /M arrest and subsequent apoptosis, and induced early apoptosis without previous cell cycle arrest at 10 -100 ng/ml in cancer cells. ET-743-mediated apoptosis, did not involve Fas/CD95. ET-743 induced c-Jun NH 2 -terminal kinase (JNK) and caspase-3 activation, and JNK and caspase inhibition prevented ET-743-induced apoptosis. ET-743 failed to promote apoptosis in caspase-3-deficient MCF-7 cells, further implicating caspase-3 in its proapoptotic action. Overexpression of bcl-2 by gene transfer abrogated ET-743-induced apoptosis, but cells underwent cell cycle arrest. ET-743 triggered cytochrome c release from mitochondria that was inhibited by Bcl-2 overexpression. Inhibition of transcription or protein synthesis did not prevent ET-743-induced apoptosis, but abrogated ET-743-induced cell cycle arrest. Microarray analyses revealed changes in the expression of a small number of cell cycle-related genes (p21, GADD45A, cyclin G2, MCM5, and histones) that suggested their putative involvement in ET-743-induced cell cycle arrest. These data indicate that ET-743 is a very potent anticancer drug showing dose-dependent cytostatic and proapoptotic effects through activation of two different signaling pathways, namely a transcriptiondependent pathway leading to cell cycle arrest and a transcription-independent route leading to rapid apoptosis that involves mitochondria, JNK, and caspase-3. Ecteinascidin-743 (ET-743)1 is a marine-derived compound isolated from the marine tunicate Ecteinascidia turbinata (1, 2), with a potent cytotoxic activity against a variety of tumors in vitro and in vivo (3-5). The preclinical in vivo experiments with ET-743 showed cytotoxic activity of the drug when administered at g/m 2 dosages, yielding nanomolar plasma concentrations (6, 7). Current phase II clinical trials in Europe and the United States indicate that ET-743 represents a highly promising antitumor agent. However, the mechanism by which ET-743 exerts its anticancer activity remains to be elucidated. ET-743 has been reported to bind to the minor groove of DNA (8, 9), bending DNA toward the major groove (10). DNA-bound ET-743 appeared to modify the interaction between DNA and several transcription factors (11,12). Also, at high concentrations ET-743 and the related synthetic drug phthalascidin, have been reported to target topoisomerase I (13, 14). However, the relevance of these actions for the antitumor activity of ET-743 can be questioned as they are evidenced at drug concentrations much higher than those required for achieving its antitumor effect. On the other hand, ET-743-treated cells have been reported to accumulate in S and G 2 /M phases (15-18).To elucidate the mechanism underlying the anticancer effect of ET-743, we investigated the putative role of apoptosis in ET-743 action as an explanation for its cytotoxic effect. In this work we have found evidence for the induction of c-Jun NH 2 -terminal kinase (JNK)-, mitoch...

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Section: Discussionsupporting

confidence: 93%

Differential Cytostatic and Apoptotic Effects of Ecteinascidin-743 in Cancer Cells

Gajate

Mollinedo

2002

Journal of Biological Chemistry

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“…Curcumin is a Michael acceptor and thus can react with sulfhydryl groups [35]. It has been shown to induce mitochondrial membrane permeability transition pores through membrane protein thiol oxidation [36]. Interestingly, curcumin was reported to form a covalent adduct with the nascent selenol/thiol of the active site of thioredoxin reductase, shifting this enzyme from an antioxidant to a pro-oxidant [37].…”

Section: Discussionmentioning

confidence: 99%

Superoxide anion and proteasomal dysfunction contribute to curcumin-induced paraptosis of malignant breast cancer cells

Yoon

Kim

Lim

et al. 2010

Free Radical Biology and Medicine

114

155

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“…It results from over production of reactive oxygen species, often leading to peroxidation of membrane phospholipids and production of reactive aldehydes (Hanasaki et al, 1994;Ferrari et al, 1996;Korshunov et al, 1997 andMorin et al, 2001). …”

Section: Discussionmentioning

confidence: 99%

Cardioprotective activity of ethanolic extract of Callistemon lanceolatus leaves on doxorubicin-induced cardiomyopathy in rats

Firoz¹,

Bharatesh²,

Nilesh³

et al. 2011

Bangladesh J Pharmacol

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The cardioprotective effect of ethanol extract of Callistemon lanceolatus leaves (100 and 200 mg/kg) against doxorubicin-induced cardiomyopathy was studied. Rats were pretreated with the extract for 7 days and simultaneous treatment with doxorubicin along with the extracts for the next 14 days. After 24 hours of last dose of doxorubicin, ECG, invasive blood pressure, serum markers (creatine kinase-MB, lactate dehydrogenase, serum transaminases), tissue anti-oxidant markers (catalase, superoxide dismutase) and extent of lipid peroxidation (malondialdehyde) were studied. The elevated ST segment, decreased blood pressure, increased level of serum enzymes and decreased level of tissue anti-oxidant markers were observed in doxorubicin treatment (p<0.01). While 200 mg/kg extract significantly reduced the elevated levels of the serum enzymes and restores the ECG and blood pressure to normal, also significantly increased the tissue anti-oxidant levels, while decreased the malondialdehyde level (p<0.01) when compared with the control. The histopathological study confirmed the cardioprotection. Article Info

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Curcumin induces the mitochondrial permeability transition pore mediated by membrane protein thiol oxidation

Cited by 151 publications

References 42 publications

Differential Cytostatic and Apoptotic Effects of Ecteinascidin-743 in Cancer Cells

Differential Cytostatic and Apoptotic Effects of Ecteinascidin-743 in Cancer Cells

Superoxide anion and proteasomal dysfunction contribute to curcumin-induced paraptosis of malignant breast cancer cells

Cardioprotective activity of ethanolic extract of Callistemon lanceolatus leaves on doxorubicin-induced cardiomyopathy in rats

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