abl-n-induced apoptosis in human breast cancer cells is partially mediated by c-jun nh2-terminal kinase activationabl-n-induced细胞凋亡在人类乳腺癌细胞部分由c-jun nh2-terminal激酶激活.pdfVIP

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abl-n-induced apoptosis in human breast cancer cells is partially mediated by c-jun nh2-terminal kinase activationabl-n-induced细胞凋亡在人类乳腺癌细胞部分由c-jun nh2-terminal激酶激活.pdf

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abl-n-induced apoptosis in human breast cancer cells is partially mediated by c-jun nh2-terminal kinase activationabl-n-induced细胞凋亡在人类乳腺癌细胞部分由c-jun nh2-terminal激酶激活

Liu et al. Breast Cancer Research 2010, 12:R9 /content/12/1/R9 RESEARCH ARTICLE Open Access ABL-N-induced apoptosis in human breast cancer cells is partially mediated by c-Jun NH2-terminal kinase activation 1 1 1 1 1 2 1* Bin Liu , Mei Han , Rong-Hua Sun , Jun-Jie Wang , Yan-Ping Zhang , Di-Qun Zhang , Jin-Kun Wen Abstract Introduction: The present study was designed to determine the possibility of acetylbritannilactone (ABL) derivative 5-(5-(ethylperoxy)pentan-2-yl)-6-methyl-3-methylene-2-oxo-2,3,3a,4,7,7a-hexahydrobenzofuran-4-yl 2-(6- methoxynaphthalen-2-yl)propanoate (ABL-N) as a novel therapeutic agent in human breast cancers. Methods: We investigated the effects of ABL-N on the induction of apoptosis in human breast cancer cells and further examined the underlying mechanisms. Moreover, tumor growth inhibition of ABL-N was done in xenograft models. Results: ABL-N induced the activation of caspase-3 in estrogen receptor (ER)-negative cell lines MDA-MB-231 and MDA-MB-468, as evidenced by the cleavage of endogenous substrate Poly (ADP-ribose) polymerase (PARP). Pretreatment of cells with pan-caspase inhibitor z-VAD-fmk or caspase-3-specific inhibitor z-DEVD-fmk inhibited ABL-N-induced apoptosis. ABL-N treatment also resulted in an increase in the expression of pro-apoptotic members (Bax and Bad) with a concomitant decrease in Bcl-2. Furthermore, c-Jun-NH2-terminal kinase (JNK) and p38 mitogen-activated protein (MAP) kinase (p38) were activated in the apoptosis induced by ABL-N and JNK-specific inhibitor SP600125 and JNK small interfering RNA (siRNA) antagonized ABL-N-mediated apoptosis. However, the p38-specific inhibitor SB203580 had no effect upon these processes. Moreover, neither of the caspase inhibit