MALAT1 Promotes the Proliferation and Metastasis of Gallbladder Cancer Cells by Activating the ERK/MAPK Pathway

Overview

Journal Cancer Biol Ther

Specialties Oncology
Pharmacology

Date 2014 Mar 25

PMID 24658096

Citations 136

Authors

Xiang-Song Wu

Xu-An Wang

Wen-Guang Wu

Yun-Ping Hu

Mao-Lan Li

Qian Ding

Hao Weng

Yi-Jun Shu

Tian-Yu Liu

Lin Jiang

Yang Cao

Run-Fa Bao

Jia-Sheng Mu

Zhu-Jun Tan

Feng Tao

Ying-Bin Liu

Affiliations

Soon will be listed here.

Abstract

Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), a long non-coding RNA (lncRNA), is associated with metastasis and is an independent prognostic factor for lung cancer. Recent studies have demonstrated that MALAT1 plays an important role in other malignancies. However, little is known about the role of MALAT1 in gallbladder carcinoma (GBC), which is the most common cancer of the biliary tract and has an extremely poor prognosis. In this study, we focused on the expression, biological functions and mechanism of MALAT1 in GBC and found that MALAT1 was significantly upregulated in GBC tissues compared with corresponding non-cancerous tissues. Knockdown of MALAT1 in GBC cell lines using lentivirus-mediated RNA interference significantly inhibited the proliferation and metastasis of the GBC cells both in vitro and in vivo. Furthermore, ERK/MAPK pathway was found to be inactivated in the GBC cell lines after MALAT1 knockdown. These results indicated that MALAT1 might serve as an oncogenic lncRNA that promotes proliferation and metastasis of GBC and activates the ERK/MAPK pathway.

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