Insulin promotes glucose consumption via regulation of miR-99a/mTOR/PKM2 pathway.

Authors

Wei Li, Department of Pathology, Cancer Center, Nanjing Medical UniversityFollow
Jing Wang, Department of Pathology, Cancer Center, Nanjing Medical UniversityFollow
Qiu-Dan Chen, Department of Pathology, Cancer Center, Nanjing Medical UniversityFollow
Xu Qian, Department of Pathology, Cancer Center, Nanjing Medical UniversityFollow
Qi Li, Department of Pathology, Cancer Center, Nanjing Medical UniversityFollow
Yu Yin, Department of Pathology, Cancer Center, Nanjing Medical UniversityFollow
Zhu-Mei Shi, Department of Neurosurgery, The First Affiliated Hospital of Nanjing Medical UniversityFollow
Lin Wang, Department of Pathology, Cancer Center, Nanjing Medical UniversityFollow
Jie Lin, Faculty of Software, Fujian Normal UniversityFollow
Ling-Zhi Liu, Department of Pathology, Anatomy and Cell Biology, Kimmel Cancer Center, Thomas Jefferson UniversityFollow
Bing-Hua Jiang, Department of Pathology, Cancer Center, Nanjing Medical University; Department of Pathology, Anatomy and Cell Biology, Kimmel Cancer Center, Thomas Jefferson UniversityFollow

Document Type

Article

Publication Date

6-10-2013

Comments

This article has been peer reviewed and is published in PLoS One.

Volume 8, Issue 6, 10 June 2013, Article numbere64924.

The published version is available at DOI: 10.1371/journal.pone.0064924. © 2013 Li et al.

Abstract

Insulin is known to regulate multiple cellular functions and is used for the treatment of diabetes. MicroRNAs have been demonstrated to be involved in many human diseases, including Type 2 diabetes. In this study, we showed that insulin decreased miR-99a expression levels, but induced glucose consumption and lactate production, and increased the expression of mTOR, HIF-1α and PKM2 in HepG2 and HL7702 cells. Forced expression of miR-99a or rapamycin treatment blocked insulin-induced PKM2 and HIF-1α expression, and glucose consumption and lactate production. Meanwhile, knockdown of HIF-1α inhibited PKM2 expression and insulin-induced glucose consumption. Taken together, these findings will reveal the role and mechanism of insulin in regulating glycolytic activities via miR-99a/mTOR.

Recommended Citation

Li, Wei; Wang, Jing; Chen, Qiu-Dan; Qian, Xu; Li, Qi; Yin, Yu; Shi, Zhu-Mei; Wang, Lin; Lin, Jie; Liu, Ling-Zhi; and Jiang, Bing-Hua, "Insulin promotes glucose consumption via regulation of miR-99a/mTOR/PKM2 pathway." (2013). Kimmel Cancer Center Faculty Papers. Paper 28.
https://jdc.jefferson.edu/kimmelccfp/28

PubMed ID

23762265