The Role and Mechanism of CircCOG5 in Regulating Ferroptosis in Ovarian Cancer Cells by Targeting miR-532-3p/LPCAT3.

IF 2.1 4区 生物学 Q4 BIOCHEMISTRY & MOLECULAR BIOLOGY
Yongfeng Guo, Min Wei, Jingjing Fan, Yulan Wang, Jing Shi, Jie Wang, Na Lu, Yuping Suo
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引用次数: 0

Abstract

This study investigated the regulatory role of CircCOG5 in the ferroptosis of ovarian cancer cells via the miR-532-3p/LPCAT3. The effects of CircCOG5 expression on proliferation, apoptosis, invasion, migration, oxidative stress, and ferroptosis of OVCAR-3 and SKOV3 cells were evaluated. CircCOG5 was lowly expressed in ovarian cancer tissues. Overexpression of CircCOG5 inhibited the proliferation, invasion, and migration of OVCAR-3 and SKOV3 cells, promoted cell oxidative stress, and aggravated apoptosis and ferroptosis. Dual luciferase assays confirmed the targeted regulation of CircCOG5 on miR-532-3p, with LPCAT3 identified as a direct target of miR-532-3p. Overexpression of CircCOG5 increased LPCAT3 expression by decreasing miR-532-3p expression in OVCAR-3 and SKOV3 cells, thereby promoting apoptosis, oxidative stress, and ferroptosis in OVCAR-3 and SKOV3 cells. Overexpression of miR-532-3p reversed the effect of overexpression of CircCOG5 on the proliferation, apoptosis, oxidative stress and ferroptosis of OVCAR-3 and SKOV3 cells. LPCAT3 overexpression antagonized the effects of miR-532-3p overexpression on the proliferation, apoptosis, oxidative stress, and ferroptosis of OVCAR-3 and SKOV3 cells. These findings suggested that CircCOG5 could modulate the ferroptosis of OVCAR-3 and SKOV3 cells through targeting regulation of miR-532-3p/LPCAT3.

CircCOG5靶向miR-532-3p/LPCAT3调控卵巢癌细胞铁下垂的作用及机制
本研究通过miR-532-3p/LPCAT3研究了CircCOG5在卵巢癌细胞铁下垂中的调节作用。观察CircCOG5表达对OVCAR-3和SKOV3细胞增殖、凋亡、侵袭、迁移、氧化应激和铁凋亡的影响。CircCOG5在卵巢癌组织中低表达。过表达CircCOG5抑制OVCAR-3和SKOV3细胞的增殖、侵袭和迁移,促进细胞氧化应激,加重细胞凋亡和铁凋亡。双荧光素酶测定证实了CircCOG5对miR-532-3p的靶向调节,LPCAT3被鉴定为miR-532-3p的直接靶点。过表达CircCOG5通过降低OVCAR-3和SKOV3细胞中miR-532-3p的表达而增加LPCAT3的表达,从而促进OVCAR-3和SKOV3细胞的凋亡、氧化应激和铁凋亡。miR-532-3p过表达逆转了CircCOG5过表达对OVCAR-3和SKOV3细胞增殖、凋亡、氧化应激和铁凋亡的影响。LPCAT3过表达可拮抗miR-532-3p过表达对OVCAR-3和SKOV3细胞增殖、凋亡、氧化应激和铁凋亡的影响。这些发现表明CircCOG5可以通过靶向调控miR-532-3p/LPCAT3来调节OVCAR-3和SKOV3细胞的铁凋亡。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Biochemical Genetics
Biochemical Genetics 生物-生化与分子生物学
CiteScore
3.90
自引率
0.00%
发文量
133
审稿时长
4.8 months
期刊介绍: Biochemical Genetics welcomes original manuscripts that address and test clear scientific hypotheses, are directed to a broad scientific audience, and clearly contribute to the advancement of the field through the use of sound sampling or experimental design, reliable analytical methodologies and robust statistical analyses. Although studies focusing on particular regions and target organisms are welcome, it is not the journal’s goal to publish essentially descriptive studies that provide results with narrow applicability, or are based on very small samples or pseudoreplication. Rather, Biochemical Genetics welcomes review articles that go beyond summarizing previous publications and create added value through the systematic analysis and critique of the current state of knowledge or by conducting meta-analyses. Methodological articles are also within the scope of Biological Genetics, particularly when new laboratory techniques or computational approaches are fully described and thoroughly compared with the existing benchmark methods. Biochemical Genetics welcomes articles on the following topics: Genomics; Proteomics; Population genetics; Phylogenetics; Metagenomics; Microbial genetics; Genetics and evolution of wild and cultivated plants; Animal genetics and evolution; Human genetics and evolution; Genetic disorders; Genetic markers of diseases; Gene technology and therapy; Experimental and analytical methods; Statistical and computational methods.
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