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miR-585-3p 通过靶向 FSCN1 阻断 MAPK 信号通路抑制卵巢癌细胞进展的功能及机制研究。

Study on the Function and Mechanism of miR-585-3p Inhibiting the Progression of Ovarian Cancer Cells by Targeting FSCN1 to Block the MAPK Signaling Pathway.

机构信息

Department of Gynecology, First Affiliated Hospital of Harbin Medical University, Harbin City, Heilongjiang Province 150001, China.

出版信息

Anal Cell Pathol (Amst). 2022 May 13;2022:1732365. doi: 10.1155/2022/1732365. eCollection 2022.

DOI:10.1155/2022/1732365
PMID:35602576
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9122712/
Abstract

Ovarian cancer (OC) is the leading cause of death for women diagnosed with gynecological cancer. Studies have shown that dysregulated miRNA expression is related to various cancers, including OC. Here, we aimed to explore the biological function and mechanism of miR-585-3p in the occurrence and development of OC. The expression level of miR-585-3p was found to be low in OC tissues and cells. We analyzed the biological function of miR-585-3p in OC through in vitro cell experiments. The results indicated that overexpression of miR-585-3p inhibited the proliferation, invasion, and migration of SW626 cells, while low expression of miR-585-3p had the opposite effect in SKOV3 cells. We then screened the target genes of miR-585-3p through miRDB database and detected the expression of target genes in OC cells. FSCN1 was found to be most significantly upregulated in OC cells. Dual-luciferase reporter assays revealed FSCN1 as a potential target of miR-585-3p. Western blot analysis showed that miR-585-3p targeted FSCN1 to inhibit protein phosphorylation of ERK. In vivo animal experiments also confirmed that miR-585-3p targets FSCN1 to inhibit tumor growth and block the MAPK signaling pathway. In summary, miR-585-3p inhibits the proliferation, migration, and invasion of OC cells by targeting FSCN1, and its mechanism of action may be achieved by inhibiting the activation of the MAPK signaling pathway. miR-585-3p may serve as a potential biomarker and therapeutic target for OC.

摘要

卵巢癌(OC)是妇科癌症患者死亡的主要原因。研究表明,miRNA 表达失调与包括 OC 在内的多种癌症有关。在这里,我们旨在探讨 miR-585-3p 在 OC 发生和发展中的生物学功能和机制。研究发现,miR-585-3p 在 OC 组织和细胞中的表达水平较低。我们通过体外细胞实验分析了 miR-585-3p 在 OC 中的生物学功能。结果表明,miR-585-3p 的过表达抑制了 SW626 细胞的增殖、侵袭和迁移,而 miR-585-3p 的低表达在 SKOV3 细胞中则有相反的效果。然后,我们通过 miRDB 数据库筛选 miR-585-3p 的靶基因,并检测 OC 细胞中靶基因的表达。结果发现,FSCN1 在 OC 细胞中表达最为显著上调。双荧光素酶报告基因实验显示 FSCN1 是 miR-585-3p 的潜在靶基因。Western blot 分析显示,miR-585-3p 通过靶向 FSCN1 抑制 ERK 蛋白磷酸化。体内动物实验也证实,miR-585-3p 通过靶向 FSCN1 抑制肿瘤生长并阻断 MAPK 信号通路。综上所述,miR-585-3p 通过靶向 FSCN1 抑制 OC 细胞的增殖、迁移和侵袭,其作用机制可能通过抑制 MAPK 信号通路的激活来实现。miR-585-3p 可能作为 OC 的潜在生物标志物和治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f804/9122712/24512181e29c/ACP2022-1732365.006.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f804/9122712/24512181e29c/ACP2022-1732365.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f804/9122712/e2ce16b91269/ACP2022-1732365.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f804/9122712/bcdd659a531b/ACP2022-1732365.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f804/9122712/0e4cf6ea07b4/ACP2022-1732365.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f804/9122712/66ed278b5971/ACP2022-1732365.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f804/9122712/2590a0ab4908/ACP2022-1732365.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f804/9122712/24512181e29c/ACP2022-1732365.006.jpg

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