1. Extracellular vesicles promote esophageal cancer progression by delivering lncZEB1-AS1 between cells.
- Author
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Zhang YG, Zhou MW, Bai L, Han RY, Lv K, and Wang Z
- Subjects
- Cell Line, Tumor, Esophageal Neoplasms genetics, Esophageal Neoplasms pathology, Extracellular Vesicles genetics, Extracellular Vesicles pathology, Gene Expression Regulation, Neoplastic, Humans, MicroRNAs genetics, MicroRNAs metabolism, RNA, Long Noncoding genetics, Signal Transduction, Zinc Finger E-box-Binding Homeobox 1 genetics, Zinc Finger E-box-Binding Homeobox 1 metabolism, Cell Proliferation, Esophageal Neoplasms metabolism, Extracellular Vesicles metabolism, RNA, Long Noncoding metabolism
- Abstract
Objective: To explore the expression of extracellular vesicle-derived lncZEB1-AS1 in esophageal cancer and its role in esophageal cancer progression., Patients and Methods: The extracellular vesicles (EVs) from esophageal cancer patients (n = 26) and normal subjects (n = 26) were isolated by differential centrifugation. The expression of lncZEB1-AS1 in EVs was detected by Real-time PCR (polymerase chain reaction). The clinical data of normal subjects and patients were analyzed. In addition, the concentration of EVs and lncZEB1-AS1 in blood samples from normal subjects and esophageal cancer patients were assessed. After co-culture of esophageal cancer cell line EC109 and EVs with or without lncZEB1-AS1 knockdown, cell proliferation was detected by CCK-8 assay. The possible target microRNAs of lncZEB1-AS1 in cytoplasm were predicted with miRcode, followed by correlation analysis of lncZEB1-AS1 and miR-214. Through literature review, lncZEB1-AS1 positively regulates ZEB1 expression, which was consistent with our result., Results: Quantitative Real-time PCR showed that the serum levels of EVs and the content of lncZEB1-AS1 in EVs from esophageal cancer patients were significantly higher than those in normal controls. LncZEB1-AS1 was overexpressed in esophageal cancer cells co-cultured with EVs of esophageal cancer patients. CCK-8 results indicated that EC109 cells co-cultured with EVs of esophageal cancer patients had stronger proliferative capacity. miRcode showed that miR-214 ranked the first of microRNAs that lncZEB1-AS1 might target, and miR-214 expression was significantly increased after lncZEB1-AS1 knockdown in EC109. After overexpressing lncZEB1-AS1 in EC109 or co-culturing EVs of esophageal cancer patients with EC109 cells, we found that lncZEB1-AS1 positively regulates ZEB1. In contrast, interfering with the expression of lncZEB1-AS1 in esophageal cancer cell lines can effectively reduce the expression of ZEB1., Conclusions: EVs in the peripheral blood from esophageal cancer patients promote esophageal cancer progression by delivering lncZEB1-AS1 to esophageal cancer cells and targeting miR-214.
- Published
- 2018
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