Roles and mechanism of miR-199a and miR-125b in tumor angiogenesis.

Authors

Jun He, State Key Lab of Reproductive Medicine, Department of Pathology, Cancer Center, Nanjing Medical UniversityFollow
Yi Jing, Department of Pathology, Anatomy and Cell Biology, Thomas Jefferson UniversityFollow
Wei Li, State Key Lab of Reproductive Medicine, Department of Pathology, Cancer Center, Nanjing Medical UniversityFollow
Xu Qian, State Key Lab of Reproductive Medicine, Department of Pathology, Cancer Center, Nanjing Medical UniversityFollow
Qing Xu, State Key Lab of Reproductive Medicine, Department of Pathology, Cancer Center, Nanjing Medical UniversityFollow
Feng-Shan Li, Department of Pathology, Nanjing Maternal and Child Care Service Center, Nanjing, Jiangsu, China
Ling-Zhi Liu, Department of Pathology, Anatomy and Cell Biology, Thomas Jefferson UniversityFollow
Bing-Hua Jiang, State Key Lab of Reproductive Medicine, Department of Pathology, Cancer Center, Nanjing Medical University; Department of Pathology, Anatomy and Cell Biology, Thomas Jefferson UniversityFollow
Yue Jiang, Faculty of Software, and College of Life Sciences, Fujian Normal UniversityFollow

Document Type

Article

Publication Date

2-20-2013

Comments

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

Volume 8, Issue 2, 20 February 2013, Article numbere56647.

The published version is available at DOI: 10.1371/journal.pone.0056647. © 2013 He et al.

Abstract

MicroRNAs (miRNAs) have been shown to be involved in different aspects of cancer biology including tumor angiogenesis. In this study, we identified that two miRNAs, miR-199a and miR-125b were downregulated in ovarian cancer tissues and cell lines. Overexpression of miR-199a and miR-125b inhibited tumor-induced angiogenesis associated with the decrease of HIF-1α and VEGF expression in ovarian cancer cells. Moreover, the levels of miR-199a and miR-125b were negatively correlated with VEGF mRNA levels in ovarian tissues. We further showed that direct targets of miR-199a and miR-125b HER2 and HER3 were functionally relevant. Forced expression of HER2 and HER3 rescued miR-199a- and miR-125b-inhibiting angiogenesis responses and Akt/p70S6K1/HIF-1α pathway. This study provides a rationale for new therapeutic approach to suppress tumor angiogenesis using miR-199a, miR-125b, or their mimics for ovarian cancer treatment in the future.

Recommended Citation

He, Jun; Jing, Yi; Li, Wei; Qian, Xu; Xu, Qing; Li, Feng-Shan; Liu, Ling-Zhi; Jiang, Bing-Hua; and Jiang, Yue, "Roles and mechanism of miR-199a and miR-125b in tumor angiogenesis." (2013). Computational Medicine Center Faculty Papers. Paper 1.
https://jdc.jefferson.edu/tjucompmedctrfp/1

PubMed ID

23437196