Circ_0050444 represses esophageal squamous cell carcinoma progression through sponging miR-486-3p to upregulate C10orf91.

IF 3.4 3区 生物学 Q3 CELL BIOLOGY Cell Cycle Pub Date : 2024-03-01 Epub Date: 2024-06-12 DOI:10.1080/15384101.2024.2357909
Dongli Zhang, Yan Zhou, Chenyang Jiao, Hongfang Kong, Zhibin Zhao, Yujiang Li
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Abstract

Esophageal squamous cell carcinoma (ESCC) ranks as the fourth leading cause of tumor-related deaths in China. Circ_0050444 has been revealed to be downregulated in ESCC tissues, however, its function and molecular mechanism underlying ESCC progression is unknown. Therefore, we attempted to clarify the functional role and molecular mechanism of circ_0050444 underlying ESCC progression. RT-qPCR and RNase R digestion assays were used to evaluate circ_0050444 expression and stability characteristics in ESCC cells. Gain-of-function assays were conducted to clarify circ_0050444 role in ESCC cell malignant behaviors. Bioinformatics and mechanism experiments were performed to assess the relationship between circ_0050444 or C10orf91 and miR-486-3p in ESCC cells. Rescue assays were conducted to evaluate the regulatory function of the circ_0050444-miR-486-3p-C10orf91 axis in ESCC cellular processes. Circ_0050444 expression was found to be downregulated both in ESCC patient tissues and cell lines. Functionally, circ_0050444 overexpression repressed ESCC cell proliferative, migratory, and invasive capabilities in cultured cells. Mechanistically, circ_0050444 was found to be competitively bound with miR-486-3p to upregulate C10orf91 in ESCC cells. Moreover, the impact of circ_0050444 elevation on ESCC cell proliferation, migration, and invasion was countervailed by C10orf91 silencing. Circ_0050444 presents downregulation and functions as a tumor suppressor in ESCC progression. Circ_0050444 suppresses ESCC proliferation, migration, and invasion through sponging miR-486-3p to upregulate C10orf91, providing a potential new direction for seeking therapeutic plans for ESCC.

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Circ_0050444 通过海绵状 miR-486-3p 上调 C10orf91 来抑制食管鳞状细胞癌的进展。
食管鳞状细胞癌(ESCC)是中国肿瘤相关死亡的第四大原因。研究发现,Circ_0050444在ESCC组织中存在下调,但其功能和分子机制尚不清楚。因此,我们试图阐明circ_0050444在ESCC进展中的功能作用和分子机制。我们采用 RT-qPCR 和 RNase R 消化试验评估了 circ_0050444 在 ESCC 细胞中的表达和稳定性特征。为了明确circ_0050444在ESCC细胞恶性行为中的作用,进行了功能增益实验。通过生物信息学和机制实验评估了 ESCC 细胞中 circ_0050444 或 C10orf91 与 miR-486-3p 之间的关系。为了评估circ_0050444-miR-486-3p-C10orf91轴在ESCC细胞过程中的调控功能,我们进行了拯救实验。研究发现,在 ESCC 患者组织和细胞系中,circ_0050444 的表达均被下调。在功能上,circ_0050444的过表达抑制了ESCC细胞在培养细胞中的增殖、迁移和侵袭能力。机理上,研究发现circ_0050444与miR-486-3p竞争性结合,上调ESCC细胞中的C10orf91。此外,Circ_0050444的升高对ESCC细胞增殖、迁移和侵袭的影响被C10orf91的沉默所抵消。Circ_0050444在ESCC进展过程中出现下调并发挥肿瘤抑制因子的功能。Circ_0050444通过海绵状miR-486-3p上调C10orf91来抑制ESCC的增殖、迁移和侵袭,为寻求ESCC的治疗方案提供了一个潜在的新方向。
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来源期刊
Cell Cycle
Cell Cycle 生物-细胞生物学
CiteScore
7.70
自引率
2.30%
发文量
281
审稿时长
1 months
期刊介绍: Cell Cycle is a bi-weekly peer-reviewed journal of high priority research from all areas of cell biology. Cell Cycle covers all topics from yeast to man, from DNA to function, from development to aging, from stem cells to cell senescence, from metabolism to cell death, from cancer to neurobiology, from molecular biology to therapeutics. Our goal is fast publication of outstanding research.
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