miR‐574‐3p inhibits proliferation and invasion in esophageal cancer by targeting FAM3C and MAPK1

Published on May 1, 2020in Kaohsiung Journal of Medical Sciences1.737
· DOI :10.1002/KJM2.12176
Ling‐Li Jin1
Estimated H-index: 1
(HUM: Hubei University of Medicine),
Shao‐Jun Zhang1
Estimated H-index: 1
(HUM: Hubei University of Medicine)
+ 3 AuthorsJie Yang1
Estimated H-index: 1
(HUM: Hubei University of Medicine)
Sources
Abstract
Esophageal cancer is considered as one of the leading malignancies. MicroRNA-574-3p (miR-574-3p) was used as a postoperative prognostic indicator in patients with esophageal squamous cell carcinoma. However, the underlying mechanism miR-574-3p involvement in esophageal cancer remains unclear. In this study, the expression of miR-574-3p was reduced in esophageal cancer tissues and cells. In vitro, miR-574-3p mimics and inhibitor were transfected into esophageal cancer cells (TE-1 and TE-8 cells) to up- or downregulating of miR-574-3p. miR-574-3p inhibited proliferation, migration and invasion, and promoted apoptosis in esophageal cancer cells. In addition, miR-574-3p was confirmed to target family with sequence similarity 3 member C (FAM3C) and mitogen-activated protein kinase 1 (MAPK1). miR-574-3p suppressed phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) and rapidly accelerated fibrosarcoma (Raf)/mitogen-activated protein kinase (MEK)/extracellular signal-regulated kinase (ERK) signaling via regulating FAM3C and MAPK1. In vivo, overexpression of miR-574-3p suppressed tumor growth in mice. Our findings indicated that miR-574-3p repressed proliferation and invasion of esophageal cancer via regulation of FAM3C and MAPK1, which provides a new biomarker for esophageal cancer treatment.
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