4.3 Article

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

Journal

OPEN MEDICINE
Volume 18, Issue 1, Pages -

Publisher

DE GRUYTER POLAND SP Z O O
DOI: 10.1515/med-2023-0630

Keywords

oral squamous cell carcinoma; circNFATC3; miR-520h; LDHA; glycolysis

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The aim of this study was to investigate the role of circNFATC3 in the development of oral squamous cell carcinoma (OSCC). The levels of circNFATC3, miR-520h, and LDHA were measured and their interactions were confirmed. Functional analysis showed that knockdown of circNFATC3 inhibited glycolysis metabolism, cell proliferation, migration, and invasion, and promoted cell apoptosis in OSCC cells. LDHA was found to regulate the development of OSCC and circNFATC3 acted as a sponge for miR-520h to modulate LDHA expression. Furthermore, the absence of circNFATC3 suppressed tumor growth in mice. In conclusion, circNFATC3 promoted the progression of OSCC through the miR-520h/LDHA axis.
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 vivo. In conclusion, circNFATC3 promoted the advancement of OSCC by adjusting the miR-520h/LDHA axis.

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