4.5 Article

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

Journal

CANCER BIOLOGY & THERAPY
Volume 15, Issue 6, Pages 806-814

Publisher

TAYLOR & FRANCIS INC
DOI: 10.4161/cbt.28584

Keywords

gallbladder carcinoma; MALAT1; lncRNA; ERK; MAPK; proliferation; metastasis

Categories

Funding

  1. National Natural Science Foundation of China [81172026, 81272402, 81301816, 81172029]
  2. National High Technology Research and Development Program (863 Program) [2012AA022606]
  3. Foundation for Interdisciplinary research of Shanghai Jiao Tong University [YG2011ZD07]
  4. Shanghai science and technology commission inter-governmental international cooperation project [12410705900]
  5. Shanghai science and technology commission medical-guiding project [12401905800]
  6. Program for Changjiang Scholars
  7. Natural Science Research Fundation of Shanghai Jiao Tong University School of Medicine [13XJ10037]
  8. Leading Talent program of Shanghai
  9. Specialized Research Fundation for PhD Program of Higher Education-Priority Development Field [20130073130014]

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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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