H3K27ac 诱导的 RNASEH1-AS1 通过招募 BUD13 稳定 ANXA2 mRNA,从而促进结直肠癌的进展。

IF 2 4区 医学 Q3 ONCOLOGY Neoplasma Pub Date : 2023-10-01 DOI:10.4149/neo_2023_230612N303
Shengwei Zhuang, Weihong Lu, Lianjun Shen, Zhekun Huang, Xiuping Zhang, Yong Zhang
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引用次数: 0

摘要

结直肠癌(CRC)是一种发病率和死亡率都很高的恶性肿瘤。lncRNA失调与CRC的发病密切相关,这一点已被广泛接受。本研究探讨了RNASEH1-AS1在CRC中的功能和机制。RT-qPCR和Western blot检测了目标基因在组织和细胞中的表达。应用 CCK-8、克隆形成、伤口愈合试验和 Transwell 法评估 CRC 细胞的恶性行为。ChIP、RIP和RNA pull-down验证了RNASEH1-AS1、H3K27ac、CBP、BUD13和ANXA2之间的相互作用。核质分离和 FISH 检测确定了 RNASEH1-AS1 在 CRC 细胞中的位置。IHC检测法用于检测小鼠肿瘤组织中Ki-67的表达。RNASEH1-AS1在CRC肿瘤组织和细胞中高表达。沉默 RNASEH1-AS1 能有效抑制 CRC 细胞的活力、增殖、迁移和侵袭。此外,CBP介导的H3K27ac增加了RNASEH1-AS1在CRC细胞中的表达,RNASEH1-AS1可通过招募BUD13提高ANXA2的表达。此外,沉默RNASEH1-AS1可通过降低ANXA2的表达和使Wnt/β-catenin通路失活来抑制CRC细胞的恶性表型和小鼠肿瘤的生长。我们的研究结果表明,CBP介导的H3K27ac诱导的RNASEH1-AS1通过招募BUD13稳定ANXA2 mRNA,激活Wnt/β-catenin通路,促进CRC的进展,这为RNASEH1-AS1在CRC中的作用提供了实质性证据。靶向RNASEH1-AS1可能会缓解CRC的进展。
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RNASEH1-AS1 induced by H3K27ac stabilizes ANXA2 mRNA to promote the progression of colorectal cancer through recruiting BUD13.

Colorectal cancer (CRC) is a malignant tumor with high morbidity and mortality. It is well-accepted that dysregulated lncRNAs are closely related to the development of CRC. In this study, the function and mechanism of RNASEH1-AS1 in CRC were investigated. RT-qPCR and western blot detected the expression of targeted genes in tissues and cells. CCK-8, clone formation, wound healing assay, and Transwell were applied to evaluate CRC cell malignant behaviors. ChIP, RIP, and RNA pull-down validated interactions among RNASEH1-AS1, H3K27ac, CBP, BUD13, and ANXA2. Nucleoplasmic separation and FISH assay determined the location of RNASEH1-AS1 in CRC cells. IHC assay was used to detect Ki-67 expression in tumor tissues from mice. RNASEH1-AS1 was highly expressed in CRC tumor tissues and cells. RNASEH1-AS1 silencing effectively suppressed the viability, proliferation, migration, and invasion of CRC cells. In addition, CBP-mediated H3K27ac increased RNASEH1-AS1 expression in CRC cells and RNASEH1-AS1 could elevate ANXA2 expression through recruiting BUD13. Furthermore, RNASEH1-AS1 silencing inhibited malignant phenotypes of CRC cells and tumor growth in mice through decreasing ANXA2 expression and inactivating the Wnt/β-catenin pathway. Our results revealed that RNASEH1-AS1 induced by CBP-mediated H3K27ac activated Wnt/β-catenin pathway to promote CRC progression through recruiting BUD13 to stabilize ANXA2 mRNA, which provides substantial evidence of RNASEH1-AS1 in CRC. Targeting RNASEH1-AS1 might alleviate CRC progression.

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来源期刊
Neoplasma
Neoplasma 医学-肿瘤学
CiteScore
5.40
自引率
0.00%
发文量
238
审稿时长
3 months
期刊介绍: The journal Neoplasma publishes articles on experimental and clinical oncology and cancer epidemiology.
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