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Ginsenoside Rg3 increases gemcitabine sensitivity of pancreatic adenocarcinoma via reducing ZFP91 mediated TSPYL2 destabilization

Pan, Haixia,Yang, Linhan,Bai, Hansong,Luo, Jing,Deng, Ying The Korean Society of Ginseng 2022 Journal of Ginseng Research Vol.46 No.5
- 원문보기 2
  DBpia
  
  ScienceON
Background: Ginsenoside Rg3 and gemcitabine have mutual enhancing antitumor effects. However, the underlying mechanisms are not clear. This study explored the influence of ginsenoside Rg3 on Zinc finger protein 91 homolog (ZFP91) expression in pancreatic adenocarcinoma (PAAD) and their regulatory mechanisms on gemcitabine sensitivity. Methods: RNA-seq and survival data from The Cancer Genome Atlas (TCGA)-PAAD and Genotype-Tissue Expression (GTEx) were used for in-silicon analysis. PANC-1, BxPC-3, and PANC-1 gemcitabine-resistant (PANC-1/GR) cells were used for in vitro analysis. PANC-1 derived tumor xenograft nude mice model was used to assess the influence of ginsenoside Rg3 and ZFP91 on tumor growth in vivo. Results: Ginsenoside Rg3 reduced ZFP91 expression in PAAD cells in a dose-dependent manner. ZFP91 upregulation was associated with significantly shorter survival of patients with PAAD. ZFP91 overexpression induced gemcitabine resistance, which was partly conquered by ginsenoside Rg3 treatment. ZFP91 depletion sensitized PANC-1/GR cells to gemcitabine treatment. ZFP91 interacted with Testis-Specific Y-Encoded-Like Protein 2 (TSPYL2), induced its poly-ubiquitination, and promoted proteasomal degradation. Ginsenoside Rg3 treatment weakened ZFP91-induced TSPYL2 poly-ubiquitination and degradation. Enforced TSPYL2 expression increased gemcitabine sensitivity of PAAD cells and partly reversed induced gemcitabine resistance in PANC-1/GR cells. Conclusion: Ginsenoside Rg3 can increase gemcitabine sensitivity of pancreatic adenocarcinoma at least via reducing ZFP91 mediated TSPYL2 destabilization.
2
Ginsenoside 20(S)-Rg3 reduces KIF20A expression and promotes CDC25A proteasomal degradation in epithelial ovarian cancer

Rong Zhang,Lei Li,Huihui Li,Hansong Bai,Yuping Suo,Ju Cui,Yingmei Wang 고려인삼학회 2024 Journal of Ginseng Research Vol.48 No.1
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  DBpia
  
  ScienceON
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.