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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
Mar 31, 2023 Vol.46 No.3, pp. 131~189
COVER PICTURE
The physiologically important cytoprotective signaling in normal cells (background area in turquoise) mediated by NRF2 (blue chain) is often hijacked by cancer cells (red ball) in the tumor microenvironment (yellow area). However, the differential roles of NRF2 throughout the multistage carcinogenesis remains largely unresolved (white-colored overlapping misty areas).

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