Cat. #152547
MCF7/LetR-1 Cell Line
Cat. #: 152547
Sub-type: Continuous
Unit size: 1x10^6 cells / vial
Organism: Human
Tissue: Breast
Disease: Cancer
£800.00
This fee is applicable only for non-profit organisations. If you are a for-profit organisation or a researcher working on commercially-sponsored academic research, you will need to contact our licensing team for a commercial use license.
Contributor
Inventor: Anne Lykkesfeldt
Institute: Danish Cancer Society
Tool Details
*FOR RESEARCH USE ONLY (for other uses, please contact the licensing team)
- Name: MCF7/LetR-1 Cell Line
- Alternate name: MCF7/LetR-1; MCF-7/S0.5/LetR-1; LetR-1
- Cancer: Breast cancer
- Cancers detailed: Breast cancer
- Research fields: Cancer;Drug development
- Tool sub type: Continuous
- Parental cell: MCF7
- Organism: Human
- Tissue: Breast
- Disease: Cancer
- Morphology: Polygonal epithelia
- Growth properties: Breast cancer cell line resistant to the aromatase inhibitor letrozole. Estrogen receptor positive. Progesterone receptor positive when grown in medium without letrozole.
- Conditional: No
- Description: MCF7/LetR-1 is a cell line model mimicking acquired resistance of aromatase inhibitors (AIs) - an anti-cancer therapy. This breast cancer cell line was established from MCF7 cells. The cellular classification is epithelial, and their shape is polygonal. The MCF7/LetR-1 cell line is resistant to the third generation AI - Letrozole (Femara). Third generation AIs have proven to be effective treatment for oestrogen receptor positive (ER+) breast cancer and as such are recommended as first line endocrine therapy for postmenopausal ER+ breast cancer patients. However, a major problem is development of resistance against AIs. Previous applications of this cell line include western blot analysis of protein expression. Since molecular mechanisms of AI resistance are largely undisclosed, the development of cell lines resistant to the non-steroidal AI Letrozole allows the study of the molecular basis for AI resistance to find new targets for treatment.
- Production details: Letrozole-resistant cell lines were established from MCF-7 cells grown in medium with 10% NCS and 10ÄË?Â?Â7 M testosterone. A culture of MCF-7 cells were treated with 10ÄË?Â?Â6 M letrozole for one week, trypsinized and seeded in serial dilutions in 24-well plates. Single colonies were transferred to new wells and gradually expanded in medium with letrozole. After ~2ÄË?Â?Â3 months, the isolated colonies gave rise to letrozole-resistant cell lines, which could be grown in letr...
- Cellosaurus id: CVCL_5A17
Target Details
- Target: Letrozole resistant
Applications
- Application notes: Human breast cancer cell line derived from MCF-7 cells Other related cell lines: - LetR-2, LetR-3 and LetR-4 resistant to the non-steroidal AI letrozole - ExeR-1, ExeR-2, ExeR-3 and ExeR-4 resistant to the steroidal AI exemestane - AnaR-1, AnaR-2, AnaR-3 and AnaR-4 resistant to the non-steroidal AI anastrozole Passage 436 (AL3117. AL3118)
Handling
- Format: Frozen
- Passage number: Passage 436 (AL3117. AL3118)
- Growth medium: Phenol-red-free DMEM/F12 medium supplemented with 10% newborn calf serum, 2.5 mM Glutamax, 6 ng/ ml insulin, 0.1 uM testosterone and 1 uM letrozole.
- Unit size: 1x10^6 cells / vial
- Shipping conditions: Dry ice
Related Tools
- Related tools: MCF7/LetR-2 Cell Line ; MCF7/LetR-4 Cell Line ; MCF7/LetR-3 Cell Line Other related cell lines: - LetR-2, LetR-3 and LetR-4 resistant to the non-steroidal AI letrozole - ExeR-1, ExeR-2, ExeR-3 and ExeR-4 resistant to the steroidal AI exemestane - AnaR-1, AnaR-2, AnaR-3 and AnaR-4 resistant to the non-steroidal AI anastrozole
References
- Hole et al. 2015. Breast Cancer Res Treat. 149(3):715-26. PMID: 25667100.
- Hole et al. 2015. Int J Oncol. 46(4):1481-90. PMID: 25625755.
- Aurora kinase A and B as new treatment targets in aromatase inhibitor-resistant breast cancer cells.
- New cell culture model for aromatase inhibitor-resistant breast cancer shows sensitivity to fulvestrant treatment and cross-resistance between letrozole and exemestane.