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Research Paper Volume 12, Issue 18 pp 18084—18098
RAI14 silencing suppresses progression of esophageal cancer via the STAT3 pathway
- 1 Department of Clinical Laboratory, The Affiliated Cancer Hospital of Nanjing Medical University and Jiangsu Cancer Hospital and Jiangsu Institute of Cancer Research, Nanjing, China
- 2 Department of Radiation Oncology, The Affiliated Cancer Hospital of Nanjing Medical University and Jiangsu Cancer Hospital and Jiangsu Institute of Cancer Research, Nanjing, China
- 3 Department of Radiotherapy, The Affiliated Changzhou No. 2 People’s Hospital with Nanjing Medical University, Changzhou, China
- 4 Department of Pharmacy, The Third Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong, China
Received: January 29, 2020 Accepted: June 13, 2020 Published: September 14, 2020
https://doi.org/10.18632/aging.103613How to Cite
Copyright: © 2020 Wang 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.
Abstract
Esophageal cancer (EC) is an aggressive malignancy that has an unclear molecular pathogenesis. Although retinoic acid induced 14 (RAI14) is involved in various cancer processes, the relationship between EC and RAI14 has not been elucidated. Our study reported the oncogenic function of RAI14 and its underlying mechanisms in EC. The Cancer Genome Atlas (TCGA) database revealed that RAI14 was upregulated in EC, and this upregulation correlated with T stage, histologic grade, and poor clinical prognosis. RAI14 was evaluated in EC cell lines, and the overexpression of RAI14 promoted cell proliferation, migration, and invasion in vitro. Conversely, RAI14 knockdown induced apoptosis and cell cycle arrest. RAI14 activated STAT3, upregulated Mcl-1 and cyclin D1, and inhibited cleaved caspase-3. Inhibition of STAT3 restored the oncogenic effect of RAI14, and RAI14 silencing restrained tumor growth and the protein level of Ki67 in vivo. Our results suggest that RAI14 regulates the STAT3 pathway and acts as an oncogene during EC progression.