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Itraconazole inhibits proliferation of pancreatic cancer cells through activation of Bak‐1
Author(s) -
Jiang Fan,
Xing HongS.,
Chen WeiY.,
Du Jie,
Ruan Yuel.,
Lin AnY.,
Zhou ChiZ.
Publication year - 2019
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.27719
Subject(s) - itraconazole , apoptosis , pancreatic cancer , in vivo , cancer research , growth inhibition , in vitro , pharmacology , chemistry , cancer cell , cancer , biology , medicine , antifungal , biochemistry , microbiology and biotechnology
Itraconazole is an FDA‐approved antifungal agent, which has been reported to possess promising anticancer activities in recent years. This study investigates the antiproliferative effects of itraconazole on pancreatic cancer cells and the molecular mechanism of its apoptosis‐inducing effects. In this study, our results showed that itraconazole inhibited the growth of pancreatic cancer cells in vitro, and it also significantly inhibited the tumor growth of CFPAC‐1 xenografts in vivo. Itraconazole induced apoptosis through ROS generation and mitochondrial membrane depolarization. A Bak‐1 activation dependent apoptosis was identified in CFPAC‐1 cells. These data suggested that itraconazole exhibited antiproliferative effects in pancreatic cancer cells by inducing apoptosis through Bak‐1 activation.