期刊
JOURNAL OF CELLULAR BIOCHEMISTRY
卷 120, 期 6, 页码 9787-9798出版社
WILEY
DOI: 10.1002/jcb.28259
关键词
apoptosis; cancer; casticin; radiation; signal transducers and activators of transcription-3
资金
- National Research Foundation of Korea [NRF-2017M3A9E4065333, NRF-2017R1A6A3A11031224, NRF-2018R1D1A1B07042969]
- KIST [2Z05140-17-149]
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.
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