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Rong Zhang,Lei Li,Huihui Li,Hansong Bai,Yuping Suo,Ju Cui,Yingmei Wang 고려인삼학회 2024 Journal of Ginseng Research Vol.48 No.1
Background: Ginsenoside 20(S)-Rg3 shows promising tumor-suppressive effects in ovarian cancer viainhibiting NF-kB signaling. This study aimed to explore the downstream tumor suppressive mechanismsof ginsenoside Rg3 via this signaling pathway. Materials and methods: A systematical screening was applied to examine the expression profile of 41kinesin family member genes in ovarian cancer. The regulatory effect of ginsenoside Rg3 on KIF20Aexpression was studied. In addition, we explored interacting proteins of KIF20A and their molecularregulations in ovarian cancer. RNA-seq data from The Cancer Genome Atlas (TCGA) was used for bioinformaticanalysis. Epithelial ovarian cancer cell lines SKOV3 and A2780 were used as in vitro and in vivocell models. Commercial human ovarian cancer tissue arrays were used for immunohistochemistrystaining. Results: KIF20A is a biomarker of poor prognosis among the kinesin genes. It promotes ovarian cancercell growth in vitro and in vivo. Ginsenoside Rg3 can suppress the transcription of KIF20A. GST pull-downand co-immunoprecipitation (IP) assays confirmed that KIF20A physically interacts with BTRC (b-TrCP1),a substrate recognition subunit for SCFb TrCP E3 ubiquitin ligase. In vitro ubiquitination and cycloheximide(CHX) chase assays showed that via interacting with BTRC, KIF20A reduces BTRC-mediated CDC25Apoly-ubiquitination and enhances its stability. Ginsenoside Rg3 treatment partly abrogates KIF20Aoverexpression-induced CDC25A upregulation. Conclusion: This study revealed a novel anti-tumor mechanism of ginsenoside Rg3. It can inhibit KIF20Atranscription and promote CDC25A proteasomal degradation in epithelial ovarian cancer.