Preclinical ReportsmiRNA-574-5p downregulates ZNF70 and influences the progression of human esophageal squamous cell carcinoma through reactive oxygen species generation and MAPK pathway activationHan, Guo Liang; Wang, Jian; Guo, Kang; Chen, Jia Kuan; Shang, Rong Xin; Jiang, TaoAuthor Information Department of chest surgery, The second affiliated hospital of Air Force Military medical University, Xi’an, Shanxi, China Received 6 April 2019 Revised form accepted 24 July 2019 Correspondence to Dr Tao Jiang, The second affiliated hospital of Air Force Military medical University, NO. 1 Xinsi Road, Xi’an 710038, Shanxi Province, China, Tel: +86 13279322357; fax: +029 89194630; e-mail: email@example.com Anti-Cancer Drugs: March 2020 - Volume 31 - Issue 3 - p 282-291 doi: 10.1097/CAD.0000000000000833 Buy Metrics Abstract There is growing evidence shown that microRNAs (miRNAs) are associated with cancer and can play a role in human cancers as oncogenes or tumor suppressor genes. miRNA-574-5p is a candidate oncogene in various types of cancer, but little is known about biological functions of miR-574-5p in esophageal squamous cell carcinoma (ESCC). In this study, we observe that the expression of miR-574-5p is not only increased in human ESCC tissues but also remarkably increased in cell lines correlates with ZNF70. In vitro, we explored the role of miR-574-5p in ESCC progression via transfection of the miR-574-5p inhibitor into ECA-109 cells. The results show miR-574-5p serve as a tumor promoter regulating cells proliferation and apoptosis in ESCC through mitochondrial-mediated reactive oxygen species (ROS) generation and MAPK pathways. Furthermore, ZNF70 has been proved to as a functional target for miR-574-5p to regulate cells poliferation and apoptosis. In summary, these results suggest that miR-574-5p serves as tumor promoter to promote proliferation and inhibit apoptosis of ESCC cells by targeting ZNF70 via mitochondrial-mediated ROS generation and MAPK pathways. The miR-574-5p/ZNF70 pathway provides a new insight into the molecular mechanisms that the occurrence and development of ESCC and it provides a novel therapeutic target for ESCC. Copyright © 2020 Wolters Kluwer Health, Inc. All rights reserved.