NU9056靶向KAT5,通过ABCE1乙酰化调控食管癌细胞的增殖、迁移和侵袭

Liang Zong-ying, Huang Jing-tao
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引用次数: 0

摘要

目的:探讨NU9056通过KAT5调控ABCE1蛋白乙酰化,影响上皮间充质转化(EMT)、增殖、迁移和侵袭的机制。方法:体外培养TE-1细胞,MTT法测定NU9056浓度,qRT-PCR法测定KAT5 mRN,免疫沉淀法测定ABCE1乙酰化,Western blot法测定KAT5和emt相关蛋白,Transwell法测定MTT、迁移和侵袭。结果:NU9056经MTT给药浓度为1.0µmol/L;NU9056组KAT5 mRNA和蛋白表达降低,ABCE1乙酰化水平降低(P<0.05);NU9056组EMT标记蛋白E-cadherin下调,N-cadherin和Slug蛋白下调(P<0.05)。NU9056组TE-1细胞存活率、迁移率、侵袭率均显著降低(P<0.05)。结论:NU9056可能通过下调KAT5表达降低ABCE1蛋白乙酰化水平,进而抑制食管癌细胞的EMT、存活、迁移和侵袭能力。关键词:乙酰转移酶抑制剂NU9056 KAT5 ABCE1;乙酰化修饰
本文章由计算机程序翻译,如有差异,请以英文原文为准。
NU9056 targets KAT5 to regulate the Proliferation, migration and invasion of esophageal cancer cells via ABCE1 acetylation
Objective: To explore the mechanism by which NU9056 affects the epithelial mesenchymal transformation (EMT), proliferation, migration, and invasion by regulating ABCE1 protein acetylation through KAT5. Methods: TE-1 cells were cultured in vitro, NU9056 concentration by MTT, KAT5 mRN by qRT-PCR, ABCE1 acetylation by immunoprecipitation, KAT5 and EMT-related proteins by Western blot, MTT, migration, and invasion by Transwell. Results: The optimal administration concentration of NU9056 was 1.0 µmol/L via the MTT. In the NU9056 group, KAT5 mRNA and protein expression decreased, and ABCE1 acetylation level decreased (P<0.05); in the NU9056 group, EMT marker protein E-cadherin was downregulated, while N-cadherin and Slug proteins were downregulated (P<0.05). TE-1 cell survival, migration, and invasion were significantly decreased in the NU9056 group (P<0.05). Conclusion: NU9056 may reduce the ABCE1 protein acetylation levels by downregulating KAT5 expression, and subsequently inhibit the EMT, survival, migration, and invasion capacity of esophageal cancer cells. Key words: Acetyltransferase inhibitor NU9056 KAT5 ABCE1, modified by acetylation
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