Clinical ReportsMicroRNA-301b and its target gene synaptosome-associated protein 91 as important modulators in esophageal cancer functional experimentsPan, Fena,,*; Chen, Mengb,,*; Song, Xin-Yanb; Yang, Jun-DongcAuthor Information aDepartment of Thoracic Surgery, Jining No. 1 People’s Hospital, Jining bDepartment of Internal Medicine, Yantai Yuhuangding Hospital of Laishan Branch, Yantai cDepartment of Radiotherapy CT, Affiliated Hospital of Jining Medical University, Jining, Shandong, People’s Republic of China * Fen Pan and Meng Chen are equally co-first authors. Xin-Yan Song is the second author. Received 10 September 2019 Revised form accepted13 December 2019 Supplemental Digital Content is available for this article. Direct URL citations appear in the printed text and are provided in the HTML and PDF versions of this article on the journal's website, www.anti-cancerdrugs.com. Correspondence to Jun-Dong Yang, Department of Radiotherapy CT, Affiliated Hospital of Jining Medical University, No. 89 Guhuai Street, Jining, Shandong 272001, People’s Republic of China, Tel:+86 133 7537 6782; fax: +86 053 7290 3051; e-mail: firstname.lastname@example.org Anti-Cancer Drugs: April 2020 - Volume 31 - Issue 4 - p 411-422 doi: 10.1097/CAD.0000000000000893 Buy SDC Metrics Abstract The aim of this study was to probe the influence of microRNA-301b (miR-301b) in esophageal cancer pathogenesis. Based on the data acquired from The Cancer Genome Atlas database, we found that miR-301b was highly expressed in esophageal cancer tissues and high expression of miR-301b was related to worse prognosis in patients with esophageal cancer. Quantitative real-time PCR revealed that the expression of miR-301b was higher in all examined esophageal cancer cell lines (ECA109, KY-SE150, TE-1, and NEC) than that in a human esophageal epithelial cell line (HEEC). Upregulation/downregulation of miR-301b facilitated/suppressed the growth, migration, and invasion of ECA109/KY-SE150 cells. Synaptosome-associated protein 91 (SNAP91) was proved to be one of the target genes of miR-301b and was negatively modulated by miR-301b. Besides, SNAP91 was lowly expressed in human esophageal cancer tissues and cell lines. Meanwhile, low expression of SNAP91 was concerned with poor prognosis in patients with esophageal cancer. Furthermore, we discovered that overexpression/depletion of SNAP91 suppressed/facilitated the proliferation of KY-SE150/ECA109 cells. MiR-301b and SNAP91 had little impact on HEEC cell proliferation and this degree of influence was negligible compared with their impacts on esophageal cancer cell proliferation. By rescue assay, we showed that overexpression of SNAP91 restrained the growth, migration, and invasion of ECA109 cells with overexpressed miR-301b while knockdown of SNAP91 showed the contrary effects on KY-SE150 cells with downregulated miR-301b. These consequences indicated that miR-301b played an important effect on esophageal cancer cells through regulating SNAP91, insinuating that miR-301b/SNAP91 might be novel potential targets for esophageal cancer therapy and prognosis. Copyright © 2020 Wolters Kluwer Health, Inc. All rights reserved.