Research Paper Volume 11, Issue 9 pp 2812—2821
LINC00857 knockdown inhibits cell proliferation and induces apoptosis via involving STAT3 and MET oncogenic proteins in esophageal adenocarcinoma
- 1 Department of Pulmonary Oncology, Affiliated Hospital of Guangdong Medical University, Zhanjiang 524023, China
- 2 Key Laboratory of Longevity and Aging-related Diseases of Chinese Ministry of Education, Center for Translational Medicine & School of Preclinical Medicine, Guangxi Medical University, Nanning, Guangxi 530021, China
- 3 , Affiliated Cancer Hospital and Institute of Guangzhou Medical University, Guangzhou 510000, China
- 4 Department of Organ Transplant, First Affiliated Hospital of Kunming Medical University, Kunming 650032, China
- 5 Section of Thoracic Surgery, Department of Surgery, University of Michigan, Ann Arbor, Michigan 48109, USA
- 6 School of Medicine, Southern University of Science and Technology, Shenzhen 518055, China
Received: December 29, 2018 Accepted: May 2, 2019 Published: May 13, 2019https://doi.org/10.18632/aging.101953
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.
Esophageal adenocarcinoma (EAC) is one of the leading causes of cancer-related death worldwide, and the molecular biology of this cancer remains poorly understood. Recent evidence indicates that long non-coding RNAs are dysregulated in a variety of cancers including EAC. In this study, siRNA mediated gene knockdown, Western blot, RT-PCR, as well as oncogenic function assay were performed. We found that the cell proliferation, colony formation, invasion and migration were decreased after LINC00857 knockdown in EAC cell lines. We also found that knockdown LINC00857 could induce apoptosis. Mechanistically, we found that the MET, STAT3, c-Myc and p-CREB proteins were decreased after LINC00857 knockdown. Our study suggests that LINC00857 may play an important oncogenic role in EAC via STAT3 and MET signaling.