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Apoptotic activity of genipin in human oral squamous cell carcinoma in vitro by regulating STAT3 signaling

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Authors

Park, Dong-Guk; Jin, Bohwan; Lee, Won W.; Kim, Hyun-Ji; Kim, Ji-Hoon; Choi, Su-Jung; Hong, Seong-Doo; Shin, Ji-Ae; Cho, Sung-Dae

Issue Date
2023-12
Publisher
John Wiley & Sons Inc.
Citation
Cell Biochemistry and Function, Vol.41 No.8, pp.1319-1329
Abstract
Genipin, a natural compound derived from the fruit of Gardenia jasminoides Ellis, was reported to have activity against various cancer types. In this study, we determined the underlying mechanism for genipin-induced cell death in human oral squamous cell carcinoma (OSCC). The growth-inhibitory effects of genipin in human OSCC cells was examined by the Cell Counting Kit-8 and soft agar assays. The effects of genipin on apoptosis were assessed by nuclear morphological changes by 4 ',6-diamidino-2-phenylindole staining, measurement of the sub-G1 population, and Annexin V-fluorescein isothiocyanate/propidium iodide double staining. The underlying mechanism of genipin activity was analyzed by western blot analysis, subcellular fractionation of the nucleus and cytoplasm, immunocytochemistry, and quantitative real-time polymerase chain reaction. Genipin inhibited the growth of OSCC cells and induced apoptosis, which was mediated by a caspase-dependent pathway. Genipin reduced the phosphorylation of signal transducer and activator of transcription 3 (STAT3) at Tyr705 and its nuclear localization. Furthermore, inhibition of p-STAT3Tyr705 levels following genipin treatment was required for the reduction of survivin and myeloid cell leukemia-1 (Mcl-1) expression, leading to apoptotic cell death. The genipin-mediated reduction in survivin and Mcl-1 expression was caused by transcriptional and/or posttranslational regulatory mechanisms. The results provide insight into the regulatory mechanism by which genipin induces apoptotic cell death through the abrogation of nuclear STAT3 phosphorylation and suggest that genipin may represent a potential therapeutic option for the treatment of human OSCC. STAT3 is frequently overexpressed in various cancers, including OSCC, indicating that it can be an oncogenic factor and cancer therapy targeting STAT3 is thought to be a promising therapeutic option.In the present study, we investigated the possibility of genipin as an anticancer drug candidate by targeting STAT3 kinase in oral cancer cell lines.The importance of our findings is genipin can mediate STAT3 signaling to induce apoptosis for treating human oral cancer and, to the best our knowledge, it is the first study showing the deactivation of STAT3 by genipin for apoptosis in oral cancer.
ISSN
0263-6484
URI
https://hdl.handle.net/10371/205166
DOI
https://doi.org/10.1002/cbf.3866
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  • School of Dentistry
  • Department of Dentistry
Research Area Discovery of molecular targets related to oral cancer metastasis and identification of signal transduction system, Identifying the role of immunological tolerance in oral cancer, Presenting a new concept oral cancer prevention and treatment strategy through identification of major molecular targets and mechanisms related to oral cancer development, 구강암 발병관련 주요 분자표적 및 기전 규명을 통한 신개념 구강암 예방 및 치료전략 제시, 구강암 전이관련 분자표적 발굴 및 신호전달체계 규명, 구강암에서 면연관용의 역할 규명

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