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Ginsenoside Rh2 reduces m6A RNA methylation in cancer via the KIF26B-SRF positive feedback loop
Chunmei Hu,Linhan Yang,Yi Wang,Shijie Zhou,Jing Luo,Yi Gu 고려인삼학회 2021 Journal of Ginseng Research Vol.45 No.6
Background: The underlying mechanisms of the potential tumor-suppressive effects of ginsenoside Rh2are complex. N6-methyladenosine (m6A) RNA methylation is usually dysregulated in cancer. This studyexplored the regulatory effect of ginsenoside Rh2 on m6A RNA methylation in cancer. Methods: m6A RNA quantification and gene-specific m6A RIP-qPCR assays were applied to assess totaland gene-specific m6A RNA levels. Co-immunoprecipitation, fractionation western blotting, andimmunofluorescence staining were performed to detect protein interactions and distribution. QRT-PCR,dual-luciferase, and ChIP-qPCR assays were conducted to check the transcriptional regulation. Results: Ginsenoside Rh2 reduces m6A RNA methylation and KIF26B expression in a dose-dependentmanner in some cancers. KIF26B interacts with ZC3H13 and CBLL1 in the cytoplasm of cancer cellsand enhances their nuclear distribution. KIF26B inhibition reduces m6A RNA methylation level in cancercells. SRF bound to the KIF26B promoter and activated its transcription. SRF mRNA m6A abundancesignificantly decreased upon KIF26B silencing. SRF knockdown suppressed cancer cell proliferation andgrowth both in vitro and in vivo, the effect of which was partly rescued by KIF26B overexpression. Conclusion: ginsenoside Rh2 reduces m6A RNA methylation via downregulating KIF26B expression insome cancer cells. KIF26B elevates m6A RNA methylation via enhancing ZC3H13/CBLL1 nuclear localization. KIF26B-SRF forms a positive feedback loop facilitating tumor growth.
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Pan, Haixia,Yang, Linhan,Bai, Hansong,Luo, Jing,Deng, Ying The Korean Society of Ginseng 2022 Journal of Ginseng Research Vol.46 No.5
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.
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