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
Correspondence to : *Correspondence: wenlong_l@yahoo.cn
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 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.
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
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
Soo-Jin Lee, Sung-E Choi, Seokho Park, Yoonjung Hwang, Youngho Son, and Yup Kang*
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