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10.1186/s12967-015-0462-8

http://scihub22266oqcxt.onion/10.1186/s12967-015-0462-8
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suck abstract from ncbi


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pmid25884389
      J+Transl+Med 2015 ; 13 (ä): 105
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  • Let-7a inhibits migration, invasion and epithelial-mesenchymal transition by targeting HMGA2 in nasopharyngeal carcinoma #MMPMID25884389
  • Wu A ; Wu K ; Li J ; Mo Y ; Lin Y ; Wang Y ; Shen X ; Li S ; Li L ; Yang Z
  • J Transl Med 2015[Mar]; 13 (ä): 105 PMID25884389 show ga
  • BACKGROUND: Let-7a has been shown to play important roles in nasopharyngeal carcinoma (NPC) cell proliferation and apoptosis, but little is known about the function and mechanism of let-7a in nasopharyngeal carcinoma metastasis. We aimed to investigate the function and mechanism of let-7a in nasopharyngeal carcinoma metastasis and clarified the regulation of high mobility group A2 (HMGA2) by let-7a. METHODS: The expression levels of let-7a and HMGA2 were examined in NPC clinical specimens using quantitative reverse transcription-PCR (RT-qPCR). HMGA2 was confirmed as a target of let-7a through luciferase reporter assays, RT-qPCR, and Western blotting. Furthermore, the roles of let-7a and HMGA2 in regulating NPC cells biological properties including proliferation, migration, invasion and epithelial-mesenchymal transition (EMT) process were analyzed with let-7a mimics and si-HMGA2 transfected cells. RESULTS: Our study demonstrated that let-7a was downregulated and inversely associated with the clinical stage, T classification and N classification, and HMGA2 was upregulated and directly associated with the clinical stage and N classification in patients with NPC. Moreover, there was an inverse correlation between let-7a expression and HMGA2 expression in NPC patient. In addition, HMGA2 was negatively regulated at the posttranscriptional level by let-7a via a binding site of HMGA2-3'UTR. In addition, synthetic let-7a mimics suppressed NPC cells migration, invasion and EMT process and knockdown of HMGA2 was consistent with the effects of let-7a in NPC cells. CONCLUSION: Let-7a directly downregulates HMGA2 protein expression, which suppress NPC cell migration, invasion and EMT process. Let-7a could serve as a potential diagnostic marker and therapeutic target for NPC.
  • |3' Untranslated Regions/genetics [MESH]
  • |Aged [MESH]
  • |Base Sequence [MESH]
  • |Carcinoma [MESH]
  • |Cell Line, Tumor [MESH]
  • |Cell Movement/*genetics [MESH]
  • |Cell Proliferation [MESH]
  • |Down-Regulation/genetics [MESH]
  • |Epithelial-Mesenchymal Transition/*genetics [MESH]
  • |Feedback, Physiological [MESH]
  • |Female [MESH]
  • |Gene Expression Regulation, Neoplastic [MESH]
  • |Gene Knockdown Techniques [MESH]
  • |HMGA2 Protein/*metabolism [MESH]
  • |Humans [MESH]
  • |Male [MESH]
  • |MicroRNAs/genetics/*metabolism [MESH]
  • |Middle Aged [MESH]
  • |Molecular Sequence Data [MESH]
  • |Nasopharyngeal Carcinoma [MESH]
  • |Nasopharyngeal Neoplasms/genetics/pathology [MESH]
  • |Neoplasm Invasiveness [MESH]
  • |Protein Binding/genetics [MESH]


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