Tropical Journal of Pharmaceutical Research

Original Research Article | OPEN ACCESS

MiR-646 targets PDK1 to recede aerobic glycolysis and cell proliferation in nasopharyngeal carcinoma

Kaiquan Zhu¹, Renyu Lin¹, Aidan Xiaguang²

¹Department of Otolaryngology, The First Affiliated Hospital of Wenzhou Medical University; ²Department of Hematology and Oncology, Wenzhou People's Hospital, Wenzhou City, Zhejiang Province 325000, China.

For correspondence:- Aidan Xiaguang Email: AidanXiadyu@163.com Tel:+8657788306139

Accepted: 30 October 2019 Published: 30 November 2019

Citation: Zhu K, Lin R, Xiaguang A. MiR-646 targets PDK1 to recede aerobic glycolysis and cell proliferation in nasopharyngeal carcinoma. Trop J Pharm Res 2019; 18(11):2299-2304 doi: 10.4314/tjpr.v18i11.10

© 2019 The authors.
This is an Open Access article that uses a funding model which does not charge readers or their institutions for access and distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0) and the Budapest Open Access Initiative (http://www.budapestopenaccessinitiative.org/read), which permit unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited..

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

Keywords: MiR-646, Aerobic glycolysis, Proliferation, PDK1, Nasopharyngeal carcinoma