Epigenetic Mechanisms of Folate Nutrition in Breast Cancer
Abstract
The most significant finding in this research period has been that making breast cancer cells folate deficient is difficult to do without killing the cells. It is much easier to target folate and one carbon metabolism in different ways such as inhibiting key enzymes with either miRNA or drugs. This is the rationale for why we have switched to making tetracycline inducible stably transduced cell lines that express miRNA against either dihydrofolate reductase (DHFR), methylenetetrahydrofolate reductase (MTHFR), s-adensoylhomocysteinase (AHCY) or DNA methyltransferase 1 (DNMT1). We have succeeded in expressing constructs containing miRNA for DHFR and AHCY in both MCF7 and MDA-MB-231 cells. The next steps involve selecting clones with non-leaky tetracycline repressor protein systems so that we can create the final tetracycline inducible, stably transduced cell lines. Once this has been accomplished we will begin to characterize the changes that occur to breast cancer cell growth and function when inhibition of either DHFR, AHCY, MTHFR or DNMT1 is induced.
Document Details
- Document Type
- Technical Report
- Publication Date
- Apr 01, 2011
- Accession Number
- ADA553202
Entities
People
- Rebecca Lobo
Organizations
- University of California