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MALAT2-activated long noncoding RNA indicates a biomarker of poor prognosis in gastric cancer.
Chen, F; Tian, Y; Pang, E-J; Wang, Y; Li, L.
Afiliação
  • Chen F; Division of General Surgery, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China.
  • Tian Y; Division of General Surgery, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China.
  • Pang EJ; Division of General Surgery, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China.
  • Wang Y; Division of General Surgery, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China.
  • Li L; Division of General Surgery, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China.
Cancer Gene Ther ; 2015 Feb 27.
Article em En | MEDLINE | ID: mdl-25721209
ABSTRACT
The purpose of this study is to investigate the role of the long noncoding RNA metastasis associated lung adenocarcinoma transcript 2 (MALAT2) in the prognosis of stage II/III gastric cancer (GC) patients. The expression of MALAT2 was evaluated in cancer tissues from 146 stage II/III GC patients undergoing radical resection and 60 paired normal samples using quantitative real-time reverse transcriptase PCR. Differences in the expression of MALAT2 between 23 GC and paired normal colonic mucosa samples were analysed with the Wilcoxon test. Relationships between the expression level of MALAT2, patient clinico-pathological parameters and disease-free survival and overall survival were analysed using the uni-variate Kaplan-Meier method and the multivariate COX regression model. The quantitative polymerase chain reaction results showed that MALAT2 was frequently over-expressed in cancer tissues and this over-expression was found to significantly correlate with lymph node metastasis and tumor stage. The ectopic expression of MALAT2 contributed to the migration of human GC SGC-7901 cells, whereas knockdown of MALAT2 inhibited the migration of the SGC-7901 cells in vitro. Further investigation into the underlying mechanisms responsible for the migratory effects revealed that MALAT2 induced the epithelial-mesenchymal transition (EMT) through an MEK/extracellular signal-regulated kinase-dependent mechanism as treatment with the MEK inhibitor, U0126, decreased migration and reversed the EMT in the MALAT2 over-expressed SGC-7901 cells. The expression of MALAT2 is upregulated in GC tissues, and a higher expression level of MALAT2 might serve as a negative prognostic marker in stage II/III GC patients which implies the potential application of MALAT2 in the therapeutic treatment of GC.Cancer Gene Therapy advance online publication, 27 February 2015; doi10.1038/cgt.2015.6.

Texto completo: 1 Base de dados: MEDLINE Tipo de estudo: Prognostic_studies Idioma: En Ano de publicação: 2015 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Tipo de estudo: Prognostic_studies Idioma: En Ano de publicação: 2015 Tipo de documento: Article