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HCT 116 ADAM17 Cell Line

Info

Catalogue Number 153209
Antigen/Gene or Protein Targets mouse ADAM17 (TACE)
Parental Line HCT 116
Host Human
Tissue Colon
Disease Keywords Colorectal cancer
Model Knock-In
Relevance Chemotherapy (5-fluorouracil) treatment has been shown to result in acute increases in transforming growth factor-α, amphiregulin, and heregulin ligand shedding in vitro and in vivo correlating with significantly increased ADAM-17 activity. Small interfering RNA–mediated 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.
Production Details HCT116 cells were cotransfected with 10 μg 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 μg/mL puromycin.
Conditional No
Research Area Cancer, Drug Discovery & Development
Growth/Phenotype Keywords Invasion, migration
Recommended Growing Conditions McCoy’s 5a Medium (GIBCO # 16600) + 10% FBS + 100 units/ml penicillin+ 100 μg/ml streptomycin
Notes Offered under licence from the Spanish National Research Council (CSIC)
Cellosaurus ID CVCL_HG03

References

There are 2 reference entries for this reagent.

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References: 2 entries

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.

Europe PMC ID: 20570921


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References: 2 entries

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.


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