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BET inhibitors synergize with sunitinib in melanoma through GDF15 suppression
Zeng Furong,Li Yayun,Meng Yu,Sun Huiyan,Yi He,Yin Mingzhu,Chen Xiang,Deng Guangtong 생화학분자생물학회 2023 Experimental and molecular medicine Vol.55 No.-
Targeting bromodomain and extra-terminal domain (BET) proteins has shown a promising therapeutic effect on melanoma. The development of strategies to better kill melanoma cells with BET inhibitor treatment may provide new clinical applications. Here, we used a drug synergy screening approach to combine JQ1 with 240 antitumor drugs from the Food and Drug Administration (FDA)-approved drug library and found that sunitinib synergizes with BET inhibitors in melanoma cells. We further demonstrated that BET inhibitors synergize with sunitinib in melanoma by inducing apoptosis and cell cycle arrest. Mechanistically, BET inhibitors sensitize melanoma cells to sunitinib by inhibiting GDF15 expression. Strikingly, GDF15 is transcriptionally regulated directly by BRD4 or indirectly by the BRD4/IL6/STAT3 axis. Xenograft assays revealed that the combination of BET inhibitors with sunitinib causes melanoma suppression in vivo. Altogether, these findings suggest that BET inhibitor-mediated GDF15 inhibition plays a critical role in enhancing sunitinib sensitivity in melanoma, indicating that BET inhibitors synergize with sunitinib in melanoma.
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Botrytis cinerea hypovirulent strain BcSpd1 induced Panax ginseng defense
Shuhan Zhang,Junyou Han,Ning Liu,Jingyuan Sun,Huchen Chen,Jinglin Xia,Huiyan Ju,Shouan Liu 고려인삼학회 2023 Journal of Ginseng Research Vol.47 No.6
Background: Gray mold, caused by Botrytis cinerea, is one of the major fungal diseases in agriculture. Biological methods are preferred over chemical fungicides to control gray mold since they are less toxicto the environment and could induce the resistance to pathogens in plants. In this work, we try tounderstand if ginseng defense to B. cinerea could be induced by fungal hypovirulent strain △BcSpd1. BcSpd1 encodes Zn(II)2Cys6 transcription factor which regulates fungal pathogenicity and we recentlyreported △BcSpd1 mutants reduced fungal virulence. Methods: We performed transcriptomic analysis of the host to investigate the induced defense responseof ginseng treated by B. cinerea △BcSpd1. The metabolites in ginseng flavonoids pathway were determinedby UPLC-ESI-MS/MS and the antifungal activates were then performed. Results: We found that △BcSpd1 enhanced the ginseng defense response when applied to healthyginseng leaves and further changed the metabolism of flavonoids. Compared with untreated plants, theapplication of △BcSpd1 on ginseng leaves significantly increased the accumulation of p-coumaric acidand myricetin, which could inhibit the fungal growth. Conclusion: B. cinerea△BcSpd1 could effectively induce the medicinal plant defense and is referred to asthe biological control agent in ginseng disease management.
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