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J Cell Biochem. 2019 Jun;120(6):9787-9798. doi: 10.1002/jcb.28259. Epub 2018 Dec 5.

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

Author information

1
Department of Science in Korean Medicine, College of Korean Medicine, Kyung Hee University, Seoul, Republic of Korea.
2
KHU-KIST Department of Converging Science and Technology, Kyung Hee University, Seoul, Republic of Korea.
3
Korean Medicine Clinical Trial Center, Korean Medicine, Hospital, Kyung Hee University, Seoul, Republic of Korea.
4
Department of Science in Korean Medicine, Kyung Hee University, Seoul, Republic of Korea.
5
Department of Radiation Oncology, Kyung Hee University Medical Center, Kyung Hee University School of Medicine, Seoul, Republic of Korea.
6
Department of Botany and Microbiology, College of Science, King Saud University, Riyadh, Saudi Arabia.
7
Department of Emergency Medicine, Pediatric Emergency Unit, College of Medicine, King Saud University, Riyadh, Saudi Arabia.
8
Department of Pharmacology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore.

Abstract

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.

KEYWORDS:

apoptosis; cancer; casticin; radiation; signal transducers and activators of transcription-3

PMID:
30520154
DOI:
10.1002/jcb.28259

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