Genetic Regulation of Lipid Biogenesis in Human Breast Cancer
Abstract
Cancer is a debilitating disease and a leading cause of death worldwide characterized by increased and uncontrolled cell growth. To accommodate their increased rates of proliferation, cancer cell membranes are typically less stable and more fluid than those of benign cells (Ntambi, 1999). The increased fluidity of the membranes may be a requirement for increased cellular proliferation, growth, and metabolism. Assessing mechanisms to normalize membrane fluidity in cancer cells may offer great therapeutic potential for cancer treatment. Stearoyl-CoA desaturase (S CD) is an oxidative enzyme crucial for the synthesis of unsaturated fatty acids. SCD inserts a cis double bond between the 9th and 10th carbons in the saturated fatty acids palmitoyl-CoA (16:0) and stearoyl-CoA (18:0) to produce palmitoleic (16:1) and oleic (18:1) acids, respectively. The monounsaturated products can then act as substrates for the synthesis of numerous cellular lipids including triglycerides, phospholipids, wax esters, and cholesterol esters. Because SCD activity increases the cellular ratio of unsaturated to saturated fatty acids, cells expressing higher levels of SCD are likely to have a higher unsaturated fatty acid component to their membranes, increasing membrane fluidity and permeability.
Document Details
- Document Type
- Technical Report
- Publication Date
- Aug 01, 2002
- Accession Number
- ADB283894
Entities
People
- James M. Ntambi
Organizations
- University of Wisconsin–Madison