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Mol. Cells 2012; 33(5): 517-524

Published online April 17, 2012

https://doi.org/10.1007/s10059-012-0022-5

© The Korean Society for Molecular and Cellular Biology

Betulinic Acid Induces Bax/Bak-Independent Cytochrome c Release in Human Nasopharyngeal Carcinoma Cells

Yang Liu, and Wenlong Luo*

E.N.T Department, The Second Affiliated Hospital of Chongqing Medical University, Chongqing City 400000, China

Correspondence to : *Correspondence: wenlong_l@yahoo.cn

Received: January 16, 2012; Revised: March 6, 2012; Accepted: March 7, 2012

Abstract

Betulinic acid (BetA) is an effective and potential anti-cancer chemical derived from plants. BetA can kill a broad range of tumor cell lines, but has no effect on untransformed cells. The chemical also kills melanoma, leukemia, lung, colon, breast, prostate and ovarian cancer cells via induction of apoptosis, which depends on caspase activation. However, no reports are yet available about the effects of BetA on nasopharyngeal carcinoma (NPC), a widely spread malignancy in the world, especially in East Asia. In this study, we first showed that BetA can effectively kill CNE2 cells, a cell line derived from NPC. BetA-induced CNE2 apoptosis was characterized by typical apoptosis hallmarks: caspase activation, DNA fragmentation, and cytochrome c release. Overexpression of Bcl-2 and Bcl-xL could partially prevent apoptosis caused by BetA. Moreover, Bax was not activated during the induction of apoptosis. Bax/Bak knockdown and wild-type CNE2 cells showed the same kinetics of cytochrome c release. We then showed that BetA may impair mitochondrial permeability transition pores (mPTPs), which may partially contribute to cytochrome c release. These observations suggest that BetA may serve as a potent and effective anti-cancer agent in NPC treatment. Further exploration of the mechanism of action of BetA could yield novel break-throughs in anti-cancer drug discovery.

Keywords apoptosis, Betulinic acid, cytochrome c release, mPTP, nasopharyngeal carcinoma

Article

Research Article

Mol. Cells 2012; 33(5): 517-524

Published online May 31, 2012 https://doi.org/10.1007/s10059-012-0022-5

Copyright © The Korean Society for Molecular and Cellular Biology.

Betulinic Acid Induces Bax/Bak-Independent Cytochrome c Release in Human Nasopharyngeal Carcinoma Cells

Yang Liu, and Wenlong Luo*

E.N.T Department, The Second Affiliated Hospital of Chongqing Medical University, Chongqing City 400000, China

Correspondence to:*Correspondence: wenlong_l@yahoo.cn

Received: January 16, 2012; Revised: March 6, 2012; Accepted: March 7, 2012

Abstract

Betulinic acid (BetA) is an effective and potential anti-cancer chemical derived from plants. BetA can kill a broad range of tumor cell lines, but has no effect on untransformed cells. The chemical also kills melanoma, leukemia, lung, colon, breast, prostate and ovarian cancer cells via induction of apoptosis, which depends on caspase activation. However, no reports are yet available about the effects of BetA on nasopharyngeal carcinoma (NPC), a widely spread malignancy in the world, especially in East Asia. In this study, we first showed that BetA can effectively kill CNE2 cells, a cell line derived from NPC. BetA-induced CNE2 apoptosis was characterized by typical apoptosis hallmarks: caspase activation, DNA fragmentation, and cytochrome c release. Overexpression of Bcl-2 and Bcl-xL could partially prevent apoptosis caused by BetA. Moreover, Bax was not activated during the induction of apoptosis. Bax/Bak knockdown and wild-type CNE2 cells showed the same kinetics of cytochrome c release. We then showed that BetA may impair mitochondrial permeability transition pores (mPTPs), which may partially contribute to cytochrome c release. These observations suggest that BetA may serve as a potent and effective anti-cancer agent in NPC treatment. Further exploration of the mechanism of action of BetA could yield novel break-throughs in anti-cancer drug discovery.

Keywords: apoptosis, Betulinic acid, cytochrome c release, mPTP, nasopharyngeal carcinoma

Mol. Cells
Sep 30, 2023 Vol.46 No.9, pp. 527~572
COVER PICTURE
Chronic obstructive pulmonary disease (COPD) is marked by airspace enlargement (emphysema) and small airway fibrosis, leading to airflow obstruction and eventual respiratory failure. Shown is a microphotograph of hematoxylin and eosin (H&E)-stained histological sections of the enlarged alveoli as an indicator of emphysema. Piao et al. (pp. 558-572) demonstrate that recombinant human hyaluronan and proteoglycan link protein 1 (rhHAPLN1) significantly reduces the extended airspaces of the emphysematous alveoli by increasing the levels of TGF-β receptor I and SIRT1/6, as a previously unrecognized mechanism in human alveolar epithelial cells, and consequently mitigates COPD.

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