Open AccessMicroRNA-338-3p suppresses tumor growth of esophageal squamous cell carcinoma in vitro and in vivo
Author(s) -
Xinyu Li,
Zhihong Li,
Guangzhong Yang,
Zhenxiang Pan
Publication year - 2015
Publication title -
molecular medicine reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.727
H-Index - 56
eISSN - 1791-3004
pISSN - 1791-2997
DOI - 10.3892/mmr.2015.3820
Subject(s) - oncogene , cancer research , carcinogenesis , cell cycle , microrna , cell growth , biology , cell , metastasis , molecular medicine , apoptosis , in vivo , cell culture , cancer , gene , biochemistry , genetics , microbiology and biotechnology
Accumulating evidence has shown that microRNAs (miRNAs) are aberrantly expressed in human esophageal squamous cell carcinoma (ESCC) and are crucial in tumorigenesis, among which miR‑338‑3p has been examined to be downregulated in patients with ESCC. However, the role of miR‑338‑3p in ESCC remains to be elucidated. In the present study, the role of miR‑338‑3p on the growth and survival of an ESCC cell line was determined with several in vitro approaches and in nude mouse models. It was determined that miR‑338‑3p expression was frequently downregulated in ESCC tissue compared with corresponding adjacent non‑tumor tissue, and that its expression was significantly correlated with tumor stage and metastasis. Overexpression of miR‑338‑3p in ESCC cells suppressed cell proliferation, colony formation, migration and invasion, and induced cell arrest at the G0/G1 stage and cell apoptosis in vitro. In addition, it was demonstrated that overexpression of miR‑338‑3p significantly suppresses tumor growth of xenograft tumors in mice (P<0.05). These findings revealed that miR‑338‑3p may act as a tumor suppressor in ESCC, and its dysregulation may be involved in the initiation and development of human ESCC. In addition, it was suggested that miR‑338‑3p may be a potential therapeutic agent for treatment of ESCC.