TargetRx Atlas

MRNA basic information

  • mRNA ID:ENST00000310823
  • Gene Name:ADAM17
  • mRNA database:Ensembl
  • mRNA expression :up-regulated
  • mRNA Method:qRT-PCR
  • mRNA Pathway:NA
  • Evidence:predicted
  • (mRNA-drug)

Drug basic information

  • Drug ID:NA
  • Drug Name:NA
  • Drug Method:NA

Disease basic infommation

  • Disease:colorectal cancer
  • Tissue:The human ileocecal colorectal adenocarcinoma cell line HCT-8 and human colorectal carcinoma cell line HCT-116 (obtained from the Cell Bank of Chinese Academy of Science) and their multidrugresistant variants HCT-8/VCR (Vincristine) and HCT-116/L-OHP (Oxa

Other information

  • Title:MiR-222 modulates multidrug resistance in human colorectal carcinoma by down-regulating ADAM-17
  • Journal:Experimental cell research
  • Published:2012
  • PubMed ID:22677042
  • Abstract:Colorectal carcinoma is a frequent cause of cancer-related death in men and women throughout the world. MicroRNAs are endogenous small noncoding RNAs that negatively regulate gene expression at the posttranscriptional level. We investigated the role of ADAM-17 (a desintegrin and metalloproteases 17) as a novel multidrug resistance (MDR) mechanism in multidrug-resistant colorectal carcinoma (CRC) and the role of miR-222 in the development of MDR in CRC cells. We found that the high expression of ADAM-17, which results in growth factor shedding and growth factor receptor activation could induce drug resistance in CRC. Pharmacological inhibition of ADAM-17, in conjunction with chemotherapy, may have therapeutic potential for the treatment of CRC. ADAM-17 is a predicted target of miR-222, which was downregulated in multidrug-resistant CRC cells. The presence of miR-222 was consistently inversely proportionate to the expression levels of ADAM-17. We found that elevated levels of miR-222 in the mimics-transfected HCT116/L-OHP and HCT-8/VCR cells reduced the ADAM-17 protein level and the luciferase activity of an ADAM-17 3＇ untranslated region-based reporter and sensitized these cells＇ apoptosis to some anticancer drugs. Our findings suggest that miR-222 could play a role in the development of MDR by modulation of ADAM-17, the new MDR treatment target in colorectal carcinoma cells.
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