Casticin inhibits growth and enhances ionizing radiation-induced apoptosis through the suppression of STAT3 signaling cascade

被引:35
|
作者
Lee, Jong Hyun [1 ]
Kim, Chulwon [1 ]
Ko, Jeong-Hyeon [1 ]
Jung, Young Yun [1 ]
Jung, Sang Hoon [2 ]
Kim, Eunok [3 ,4 ]
Kong, Moonkyoo [5 ]
Chinnathambi, Arunachalam [6 ]
Alahmadi, Tahani Awad [6 ,7 ]
Alharbi, Sulaiman Ali [6 ]
Sethi, Gautam [8 ]
Ahn, Kwang Seok [1 ,2 ]
机构
[1] Kyung Hee Univ, Coll Korean Med, Dept Sci Korean Med, Seoul, South Korea
[2] Kyung Hee Univ, KHU KIST Dept Converging Sci & Technol, Seoul, South Korea
[3] Kyung Hee Univ, Korean Med Hosp, Korean Med Clin Trial Ctr, Seoul, South Korea
[4] Kyung Hee Univ, Dept Sci Korean Med, Seoul, South Korea
[5] Kyung Hee Univ, Sch Med, Med Ctr, Dept Radiat Oncol, Seoul, South Korea
[6] King Saud Univ, Dept Bot & Microbiol, Coll Sci, Riyadh, Saudi Arabia
[7] King Saud Univ, Dept Emergency Med, Coll Med, Pediat Emergency Unit, Riyadh, Saudi Arabia
[8] Natl Univ Singapore, Yong Loo Lin Sch Med, Dept Pharmacol, Singapore 117600, Singapore
基金
新加坡国家研究基金会;
关键词
apoptosis; cancer; casticin; radiation; signal transducers and activators of transcription-3; HUMAN HEPATOCELLULAR-CARCINOMA; CERVICAL-CANCER CELLS; DEATH RECEPTOR 5; NF-KAPPA-B; TUMOR-GROWTH; VITEX-ROTUNDIFOLIA; DOWN-REGULATION; POTENTIAL ROLE; BREAST-CANCER; ACTIVATION;
D O I
10.1002/jcb.28259
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Casticin (CTC), one of the major components of Vitex rotundifolia L., has been reported to exert significant beneficial pharmacological activities and can function as an antiprolactin, anticancer, anti-inflammatory, neuroprotective, analgesic, and immunomodulatory agent. This study aimed at investigating whether the proapoptotic effects of CTC may be mediated through the abrogation of signal transducers and activators of transcription-3 (STAT3) signaling pathway in a variety of human tumor cells. We found that CTC significantly decreased cell viability in a concentration-dependent manner and suppressed cell proliferation in 786-O, YD-8, and HN-9 cells. CTC also induced programmed cell death that was found to be mediated via caspase-3 activation and induction of poly(ADP-ribose) polymerase cleavage. Interestingly, CTC repressed both constitutive and interleukin-6-induced STAT3 activation in 786-O and YD-8 cells but only affected constitutive STAT3 phosphorylation in HN-9 cells. Moreover, CTC could potentiate ionizing radiation-induced apoptotic effects leading to the downregulation of STAT3 activation and thus may be used in combination with radiation against diverse malignancies.
引用
收藏
页码:9787 / 9798
页数:12
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