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Contributor Information

  • Name Sandra Van Schaeybroeck
  • Institute Queen's University Belfast

Tool Details

  • Tool name: HCT 116 ADAM17 Cell Line
  • Tool type: Cell Lines
  • Tool sub-type: Continuous
  • Parental cell line: HCT 116
  • Organism: Human
  • Tissue: Colon
  • Cancer type: Digestive / Gastrointestinal cancer
  • Disease: Cancer
  • Growth properties: Invasion, migration
  • Model: Knock-In
  • Conditional: No
  • Description: Chemotherapy (5-fluorouracil) treatment has been shown to result in acute increases in transforming growth factor-a, amphiregulin, and heregulin ligand shedding in vitro and in vivo correlating with significantly increased ADAM-17 activity. Small interfering RNAmediated silencing and pharmacologic inhibition confirmed that ADAM-17 was the principal ADAM involved in this prosurvival response. HCT 116 ADAM17 Cell Line showed that overexpression of ADAM-17 significantly decreases the effect of chemotherapy on tumor growth and apoptosis.
  • Research area: Cancer; Drug development
  • Production details: HCT116 cells were cotransfected with 10 ÎĚ?Ÿg of a plasmid containing hemagglutinin (HA)-tagged full-length mouse ADAM-17 (HA-ADAM-17) and a construct expressing a puromycin resistance gene. Stably transfected cells were selected and maintained in medium supplemented with 1 ÎĚ?Ÿg/mL puromycin.
  • Cellosaurus ID: CVCL_HG03
  • Additional notes: Offered under licence from the Spanish National Research Council (CSIC)

  • For Research Use Only

Target Details

  • Target: mouse ADAM17 (TACE)

Application Details


  • Format: Frozen
  • Growth medium: McCoy's 5a Medium (GIBCO # 16600) + 10% FBS + 100 units/ml penicillin+ 100 ?g/ml streptomycin
  • Shipping conditions: Dry ice



  •   Kyula et al. 2010. Clin Cancer Res. 16(13):3378-89. PMID: 20570921.
  •   Chemotherapy-induced activation of ADAM-17: a novel mechanism of drug resistance in colorectal cancer.