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Published:
Jul 7, 2021Keywords:
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Main Article Content
MiR-646 targets PDK1 to recede aerobic glycolysis and cell proliferation in nasopharyngeal carcinoma
Abstract
Purpose: To investigate the effect and mechanism of miR-646 on aerobic glycolysis and cell proliferation in nasopharyngeal carcinoma.
Methods: MiR-646 expression in human nasopharyngeal carcinoma cell lines was determined by quantitative real-time polymerase chain reaction) (qRT-PCR). Cell counting kit-8 (CCK8) was used to evaluate cell viability, and colony formation assay was also performed. The target of miR-646 was determined by luciferase activity assay. The effect of miR-646 on aerobic glycolysis was assessed via glucose uptake, and lactate and ATP production. Western blot analysis was conducted to unravel the underlying mechanism involved in the regulation of miR-646 in nasopharyngeal carcinoma.
Results: MiR-646 was downregulated in human nasopharyngeal carcinoma cell lines. MiR-646 mimics decreased cell viability and inhibited cell proliferation, whereas miR-646 inhibitor increased cell viability and promoted cell proliferation. Pyruvate dehydrogenase kinase 1(PDK1) was identified as a target of miR-646, and its expression was negatively regulated by miR-646. MiR-646 probably inhibited aerobic glycolysis via regulation of PDK1, as shown by decreased glucose uptake and decreased lactate and ATP production. The inhibitory effect of miR-646 on nasopharyngeal carcinoma cell proliferation was partly via PDK1 regulation.
Conclusion: MiR-646 inhibits aerobic glycolysis in nasopharyngeal carcinoma and promotes cell proliferation via suppression of PDK1, suggesting miR-646 as a potential therapeutic target in nasopharyngeal carcinoma.
