Research Paper Volume 11, Issue 13 pp 4587—4596
LncRNA MIR22HG abrogation inhibits proliferation and induces apoptosis in esophageal adenocarcinoma cells via activation of the STAT3/c-Myc/FAK signaling
- 1 Department of Oncology, Affiliated Hospital of Guangdong Medical University, Zhanjiang, China
- 2 Department of Surgery, University of Michigan, Ann Arbor, Ann Arbor, MI 48109, USA
- 3 Key Laboratory of Longevity and Aging-related Diseases of Chinese Ministry of Education, Center for Translational Medicine and School of Preclinical Medicine, Guangxi Medical University, Nanning, China
- 4 Department of Respiratory and Critical Care Medicine, The Second Affiliated Hospital of Xian Jiaotong University, Xi’an, China
- 5 Affiliated Cancer Hospital and Institute of Guangzhou Medical University, Guangzhou, China
- 6 Department of Organ Transplant, First Affiliated Hospital of Kunming Medical University, Kunming, China
- 7 School of Medicine, Southern University of Science and Technology, Shenzhen, China
Received: December 18, 2018 Accepted: June 28, 2019 Published: July 10, 2019https://doi.org/10.18632/aging.102071
How to Cite
Copyright: Su et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Long non-coding RNAs (lncRNAs) have involved in human malignancies and played an important role in gene regulations. The dysregulation of lncRNA MIR22HG has been reported in several cancers. However, the role of MIR22HG in esophageal adenocarcinoma (EAC) is poorly understood. Loss of function approaches were used to investigate the biological role of MIR22HG in EAC cells. The effects of MIR22HG on cell proliferation were evaluated by WST-1 and colony formation assays. The effects of MIR22HG on cell migration and invasion were examined using transwell assays. QRT-PCR and Western blot were used to evaluate the mRNA and protein expression of related genes. In this study, abrogation of MIR22HG inhibited cell proliferation, colony formation, invasion and migration in EAC 3 cell lines (OE33, OE19 and FLO-1). Mechanistically, MIR22HG silencing decreased the expression of STAT3/c-Myc/p-FAK proteins and induced apoptosis in EAC cell lines. These results delineate a novel mechanism of MIR22HG in EAC, and may provide potential targets by developing lncRNA-based therapies for EAC.