Open AccessmiR‐574‐3p inhibits proliferation and invasion in esophageal cancer by targeting FAM3C and MAPK1
Author(s) -
Jin LingLi,
Zhang ShaoJun,
Lu GuangXin,
Lv Fei,
Shang Rui,
Yang Jie
Publication year - 2020
Publication title -
the kaohsiung journal of medical sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.439
H-Index - 36
eISSN - 2410-8650
pISSN - 1607-551X
DOI - 10.1002/kjm2.12176
Subject(s) - medicine , cancer research , esophageal cancer , pi3k/akt/mtor pathway , protein kinase b , mapk/erk pathway , protein kinase a , microrna , cell growth , cancer , kinase , transfection , signal transduction , cell culture , microbiology and biotechnology , biology , biochemistry , genetics , gene
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.