Journal
LIFE SCIENCES
Volume 278, Issue -, Pages -Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.lfs.2021.119491
Keywords
Esophageal cancer; MicroRNA-19b-3p; Suppressor of cytokine signaling 1; Proliferation; Apoptosis; Bone marrow mesenchymal stem cells-derived exosome
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BMSC-derived exosomal miR-19b-3p promotes progression of esophageal cancer (EC) by targeting SOCS1. This study provides a novel understanding on the molecular mechanisms of EC.
Objective: Exosomes can convey particular microRNAs (miRNAs) to affect biological functions of cancer cells. Nevertheless, the impact of bone marrow mesenchymal stem cells (BMSCs)-derived exosomes (BMSC-exos) transmitting miR-19b-3p on esophageal cancer (EC) progression remains scarcely studied. We aimed to explore the role of BMSC-exos mediating miR-19b-3p in EC cell growth. Methods: Eighty-three cases of EC patients were included in this study and the expression of miR-19b-3p and suppressor of cytokine signaling 1 (SOCS1) in cancer and adjacent normal tissues from the patients were assessed. BMSCs were cultured and BMSC-exos were extracted, which were then transfected with altered miR19b-3p and SOCS1 to assess their roles in proliferation, migration, invasion, epithelial-mesenchymal transition (EMT) and apoptosis of EC cells. Targeting relationship between miR-19b-3p and SOCS1 was verified by Targetscan and dual luciferase reporter gene assay. MiR-19b-3p and SOCS1 expression was assessed in TE-2 cells. Results: MiR-19b-3p was upregulated and SOCS1 was downregulated in EC tissues. BMSC-exos or exosomal miR19b-3p promoted malignant behaviors of EC cells. MiR-19b-3p was upregulated and targeted SOCS1 in EC cells. MiR-19b-3p inhibition or SOCS1 overexpression suppressed proliferation, migration, invasion and EMT, and induced apoptosis of EC cells. SOCS1 silencing abrogated these effect of miR-19b-3p inhibition on EC cells. Conclusion: BMSC-derived exosomal miR-19b-3p promotes progression of EC through targeting SOCS1. This study provides a novel understanding on molecular mechanisms of EC.
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