MALAT1 promotes the proliferation and metastasis of gallbladder cancer cells by activating the ERK/MAPK pathway

Xiangsong Wu(Shanghai Jiao Tong University), Xu-An Wang(Shanghai Jiao Tong University), Wenguang Wu(Shanghai Jiao Tong University), Yunping Hu(Shanghai Jiao Tong University), Maolan Li(Shanghai Jiao Tong University), Qian Ding(Shanghai Jiao Tong University), Hao Weng(Shanghai Jiao Tong University), Yijun Shu(Shanghai Jiao Tong University), Tianyu Liu(Shanghai Jiao Tong University), Lin Jiang(Shanghai Jiao Tong University), Yang Cao(Shanghai Jiao Tong University), Runfa Bao(Shanghai Jiao Tong University), Jiasheng Mu(Shanghai Jiao Tong University), Zhujun Tan(Shanghai Jiao Tong University), Feng Tao(Shaoxing No.6 People's Hospital), Yingbin Liu(Shanghai Jiao Tong University)
Cancer Biology & Therapy
March 21, 2014
Cited by 232Open Access
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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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