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

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

  • J Cell Biochem. 2019 Jun;120(6):9787-9798. doi: 10.1002/jcb.28259.
Jong Hyun Lee 1,  Chulwon Kim 1,  Jeong-Hyeon Ko 1,  Young Yun Jung 1,  Sang Hoon Jung 2,  Eunok Kim 3 4,  Moonkyoo Kong 5,  Arunachalam Chinnathambi 6,  Tahani Awad Alahmadi 6 7,  Sulaiman Ali Alharbi 6,  Gautam Sethi 8,  Kwang Seok Ahn 1 2
Affiliations

Affiliations

  • 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.
PMID: 30520154 DOI: 10.1002/jcb.28259
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.

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