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10.18632/oncotarget.3835

http://scihub22266oqcxt.onion/10.18632/oncotarget.3835
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C4558147!4558147 !25945841
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suck abstract from ncbi


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pmid25945841
      Oncotarget 2015 ; 6 (17 ): 15222-34
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  • MiR-338-3p inhibits epithelial-mesenchymal transition in gastric cancer cells by targeting ZEB2 and MACC1/Met/Akt signaling #MMPMID25945841
  • Huang N ; Wu Z ; Lin L ; Zhou M ; Wang L ; Ma H ; Xia J ; Bin J ; Liao Y ; Liao W
  • Oncotarget 2015[Jun]; 6 (17 ): 15222-34 PMID25945841 show ga
  • MicroRNAs (miRNAs) are involved in the epithelial-mesenchymal transition (EMT) process and are associated with metastasis in gastric cancer (GC). MiR-338-3p has been reported to be aberrantly expressed in GC. In the present study, we show that miR-338-3p inhibited the migration and invasion of GC cells in vitro. Knocking down miR-338-3p in GC cells led to mesenchymal-like changes. MiR-338-3p influenced the expression of the EMT-associated proteins by upregulating the epithelial marker E-cadherin and downregulating the mesenchymal markers, N-cadherin, fibronectin, and vimentin. In terms of mechanism, miR-338-3p directly targeted zinc finger E-box-binding protein 2 (ZEB2) and metastasis-associated in colon cancer-1 (MACC1). MiR-338-3p repressed the Met/Akt pathway after MACC1 inhibition. Reintroduction of ZEB2 and MACC1 reversed miR-338-3p-induced EMT suppression. Consistently, inverse correlations were also observed between the expression of miR-338-3p and ZEB2 or MACC1 in human GC tissue samples. In conclusion, miR-338-3p inhibited the EMT progression in GC cells by targeting ZEB2 and MACC1/Met/Akt signaling.
  • |Cadherins/biosynthesis [MESH]
  • |Cell Line, Tumor [MESH]
  • |Cell Movement [MESH]
  • |Epithelial-Mesenchymal Transition/*genetics [MESH]
  • |Fibronectins/biosynthesis [MESH]
  • |HEK293 Cells [MESH]
  • |Homeodomain Proteins/*genetics [MESH]
  • |Humans [MESH]
  • |MicroRNAs/*genetics [MESH]
  • |Neoplasm Invasiveness/genetics [MESH]
  • |Neoplasm Metastasis/genetics/pathology [MESH]
  • |Protein Binding [MESH]
  • |Proto-Oncogene Proteins c-akt/genetics/metabolism [MESH]
  • |Proto-Oncogene Proteins c-met/genetics/metabolism [MESH]
  • |Repressor Proteins/*genetics [MESH]
  • |Signal Transduction/genetics [MESH]
  • |Stomach Neoplasms/genetics/*pathology [MESH]
  • |Trans-Activators [MESH]
  • |Transcription Factors/*genetics/metabolism [MESH]
  • |Vimentin/biosynthesis [MESH]


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