HCT 116 ADAM17 Cell Line

HCT 116 ADAM17 Cell Line showed that overexpression of ADAM-17 significantly decreases the effect of chemotherapy on tumor growth and apoptosis.

Contributors

Inventor Institute
Sandra Van Schaeybroeck Queen's University Belfast
Cat. #: 153209
Tool sub type: Continuous
Unit size: 1×10^6 cells / vial
Cancer types: Digestive / Gastrointestinal cancer
Research Fields: Cancer;Drug development
Organism: Human
Tissue: Colon
Model: Knock-In
Growth properties: Invasion, migration
Cancer Types In Detail: Colorectal
Product 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.
Conditional: No
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.
Additional notes: Offered under licence from the Spanish National Research Council (CSIC)
Cellosaurus ID: CVCL_HG03
Parental cell line: HCT 116
disease: Cancer
Format: Frozen
Shipping conditions: Dry ice
Growth medium: McCoy's 5a Medium (GIBCO # 16600) + 10% FBS + 100 units/ml penicillin+ 100 ?g/ml streptomycin
Recommended controls: HCT 116 parental line
References:

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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