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环状核因子活化T细胞胞浆蛋白3通过miR-520h/乳酸脱氢酶A轴促进口腔鳞状细胞癌的进展。

circNFATC3 facilitated the progression of oral squamous cell carcinoma via the miR-520h/LDHA axis.

作者信息

Xie Hongguo, Lu Xiaopeng

机构信息

Department of Stomatology, Jingmen No. 1 People's Hospital, Jingmen, 448000, Hubei, China.

Department of Stomatology, Jingmen No. 1 People's Hospital, No. 168, Xiangshan Avenue, Duodao District,, Jingmen, 448000, Hubei, China.

出版信息

Open Med (Wars). 2023 Jun 27;18(1):20230630. doi: 10.1515/med-2023-0630. eCollection 2023.

Abstract

The aim of this study was to verify the effects of circular RNA nuclear factor of activated T-cells, cytoplasmic 3 (circNFATC3), in oral squamous cell carcinoma (OSCC) development. The levels of circNFATC3, microRNA-520h (miR-520h), and lactate dehydrogenase A (LDHA) were measured by qRT-PCR and western blot analysis. The cellular functions were assessed by using commercial kits, MTT assay, EdU assay, flow cytometry analysis, and transwell assay. The interactions between miR-520h and circNFATC3 or LDHA were confirmed by dual-luciferase reporter assay. Finally, the mice test was enforced to evaluate the character of circNFATC3. We observed that the contents of circNFATC3 and LDHA were upregulated and miR-520h levels were downregulated in OSCC tissues compared with those in paracancerous tissues. For functional analysis, circNFATC3 knockdown repressed the cell glycolysis metabolism, cell proliferation, migration, and invasion, although it improved cell apoptosis in OSCC cells. LDHA could regulate the development of OSCC. circNFATC3 acted as a miR-520h sponge to modulate LDHA expression. In addition, the absence of circNFATC3 subdued tumor growth . In conclusion, circNFATC3 promoted the advancement of OSCC by adjusting the miR-520h/LDHA axis.

摘要

本研究旨在验证环状RNA活化T细胞核因子细胞质3(circNFATC3)在口腔鳞状细胞癌(OSCC)发生发展中的作用。通过qRT-PCR和蛋白质免疫印迹分析检测circNFATC3、微小RNA-520h(miR-520h)和乳酸脱氢酶A(LDHA)的水平。使用商业试剂盒、MTT法、EdU法、流式细胞术分析和Transwell法评估细胞功能。通过双荧光素酶报告基因检测证实miR-520h与circNFATC3或LDHA之间的相互作用。最后,进行小鼠实验以评估circNFATC3的特性。我们观察到,与癌旁组织相比,OSCC组织中circNFATC3和LDHA的含量上调,而miR-520h水平下调。功能分析表明,敲低circNFATC3可抑制OSCC细胞的糖酵解代谢、细胞增殖、迁移和侵袭,尽管它促进了细胞凋亡。LDHA可调节OSCC的发展。circNFATC3作为miR-520h的海绵来调节LDHA的表达。此外,circNFATC3的缺失抑制了肿瘤生长。总之,circNFATC3通过调节miR-520h/LDHA轴促进了OSCC的进展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bff4/10308242/c7579392223b/j_med-2023-0630-fig001.jpg

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