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Differential expression profiling of microRNAs in para-carcinoma, carcinoma and relapse human pancreatic cancer

  • X.-L. Lai [1] ; Y.-H. Huang [4] ; Y.-S. Li [5] ; G.-N. Li [2] ; L.-P. Wang [4] ; R. Sun [4] ; Y.-S. Ma [3] ; S.-Y. Feng [3] ; Z.-Y. Chang [1] ; X.-H. Wang [6] ; D. Fu [1] ; X. Han [6] ; X.-L. Cong [4] ; W.-P. Li [1]
    1. [1] Hunan Agricultural University

      Hunan Agricultural University

      China

    2. [2] Beihua University

      Beihua University

      China

    3. [3] Shanghai Tenth People's Hospital

      Shanghai Tenth People's Hospital

      China

    4. [4] China-Japan Union Hospital, China
    5. [5] Xiangya Hospital, China
    6. [6] General Hospital of Administration Bureau for Petrolium of North China, China
  • Localización: Clinical & translational oncology, ISSN 1699-048X, Vol. 17, Nº. 5 (May 2015), 2015, págs. 398-408
  • Idioma: inglés
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  • Resumen
    • Purpose To explore the altered different expression of miRNAs and the mechanisms underlying the relapse and metastasis of pancreatic cancer.

      Materials and methods The most differentially expressed miRNAs were analyzed by gene ontology (GO) term analysis, Kyoto encyclopedia of genes and genomes (KEGG) pathway analysis and protein interaction analysis. The potentially regulated target genes of the most differentially expressed miRNAs were also analyzed further by GO term analysis and KEGG pathway analysis, and quantitated by qRT-PCR.

      Results In total, we found 12 miRNAs displayed at least a 30-fold increase or decrease in expression of carcinoma and relapse vs. para-carcinoma human pancreatic cancer (C/R vs. P). In addition, our study found that pancreatic cancer was related to pathways in cancer, including Jak-STAT signaling pathway, MAPK signaling pathway and PPAR signaling pathway.

      Conclusions The differential expressed miRNAs and their predicted target genes that involved in Jak-STAT signaling pathway, MAPK signaling pathway and PPAR signaling pathway indicating their potential roles in pancreatic carcinogenesis and progress.


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