dc.contributor.author | Hong, Ming | |
dc.contributor.author | Lee, Selena | |
dc.contributor.author | Clayton, Jacob | |
dc.contributor.author | Yake, Wildman | |
dc.contributor.author | Li, Jinke | |
dc.date.accessioned | 2020-11-11T16:26:07Z | |
dc.date.available | 2020-11-11T16:26:07Z | |
dc.date.issued | 2020-08-02 | |
dc.identifier.citation | Hong, M., Lee, S., Clayton, J., Yake, W., & Li, J. (2020). Genipin suppression of growth and metastasis in hepatocellular carcinoma through blocking activation of STAT-3. Journal of experimental & clinical cancer research : CR, 39(1), 146. https://doi.org/10.1186/s13046-020-01654-3 | en_US |
dc.identifier.uri | http://hdl.handle.net/1808/30835 | |
dc.description | This work is licensed under a Creative Commons Attribution 4.0 International License. | en_US |
dc.description.abstract | Background
The signal transducer and activator of transcription-3 (STAT-3) can facilitate cancer progression and metastasis by being constitutively active via various signaling. Abundant evidence has indicated that STAT-3 may be a promising molecular target for cancer treatment.Methods
In this study, a dual-luciferase assay-based screening of 537 compounds for STAT-3 inhibitors of hepatocellular carcinoma (HCC) cells was conducted, leading to the identification of genipin. Effects of genipin on HCC were assessed in a patient-derived xenograft nude mice model. Western blotting assay, chromatin immunoprecipitation (ChIP) assay, molecular docking study, tube formation assay, three-dimensional top culture assay, histological examination, and immunofluorescence were utilized to evaluate the regulatory signaling pathway.Results
Our research demonstrated that genipin suppresses STAT-3 phosphorylation and nuclear translocation, which may be attributed to the binding capacity of this compound to the Src homology-2 (SH2) domain of STAT-3. In addition, the therapeutic effects of genipin in a patient-derived HCC xenograft nude mice model were also demonstrated.Conclusions
In conclusion, genipin showed therapeutic potential for HCC treatment by interacting with the SH2-STAT-3 domain and suppressing the activity of STAT-3. In the future, further research is planned to explore the potential role of genipin in combination with chemotherapy or radiotherapy for HCC. | en_US |
dc.description.sponsorship | Xing-lin Foundation (GZF-1366732 K) | en_US |
dc.description.sponsorship | NIH NS79432 | en_US |
dc.publisher | BMC | en_US |
dc.rights | Copyright © 2020, The Author(s) | en_US |
dc.rights.uri | http://creativecommons.org/licenses/by/4.0/ | en_US |
dc.title | Genipin suppression of growth and metastasis in hepatocellular carcinoma through blocking activation of STAT-3 | en_US |
dc.type | Article | en_US |
kusw.kuauthor | Hong, Ming | |
kusw.kuauthor | Lee, Selena | |
kusw.kuauthor | Clayton, Jacob | |
kusw.kuauthor | Yake, Wildman | |
kusw.kuauthor | Li, Jinke | |
kusw.kudepartment | Pharmacology & Toxicology | en_US |
dc.identifier.doi | 10.1186/s13046-020-01654-3 | en_US |
kusw.oaversion | Scholarly/refereed, publisher version | en_US |
kusw.oapolicy | This item meets KU Open Access policy criteria. | en_US |
dc.identifier.pmid | PMC7397684 | en_US |
dc.rights.accessrights | openAccess | en_US |