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Casticin inhibits growth and enhances ionizing radiation–induced apoptosis through the suppression of STAT3 signaling cascade
Author(s) -
Lee Jong Hyun,
Kim Chulwon,
Ko JeongHyeon,
Jung Young Yun,
Jung Sang Hoon,
Kim Eunok,
Kong Moonkyoo,
Chinnathambi Arunachalam,
Alahmadi Tahani Awad,
Alharbi Sulaiman Ali,
Sethi Gautam,
Ahn Kwang Seok
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.28259
Subject(s) - stat3 , apoptosis , chemistry , signal transduction , viability assay , microbiology and biotechnology , poly adp ribose polymerase , downregulation and upregulation , cell growth , cancer research , stat , biology , biochemistry , polymerase , gene
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.