Analysis of Tumor Surveillance: Comparison of 10ME and L88.3 Cell Lines Through the Analysis of DNA Microarrays

Abstract

Cancer has become one of the most prevalent health issues in contemporary society. However, the exact steps or stages that a cell takes from normal to cancerous has yet to be discerned. B/CN, 10ME, and L88.3 are cell lines derived as a lineage representing the progression of a cell from normal to intermediate to a cancerous phenotype. This study seeks to compare two cell lines, 10ME and L88.3, to examine the differences in gene expression between a cell line capable of forming tumors only in immunodeficient mice, 10ME, and one that is capable of tumor formation in normal mice (L88.3). Additionally, I examined gene expression in these cell lines following treatment with tumor necrosis factor (TNF). TNF is a member of a family of protein ligands that cause cytotoxicity in certain cells and is the effector molecule associated with natural cytotoxic (NC) cells. Based on Burnet’s theory of immune surveillance of tumors, the cell line 10ME can be considered intermediate on the pathway to cancer in that it is tumorigenic in immune deficient mice but rejected by normal mice. L88.3, derived from 10ME, is tumorigenic in normal mice and thus has escaped immune surveillance. I compared these genetic profiles of these two cell lines in an attempt to reveal molecular mechanisms that show a close relationship with cells that progress from surveillance-susceptible to tumorigenic in normal mice. Comparison of these cell lines using DNA microarrays has revealed several clusters of genes with similar molecular functions in related pathways, including genes that code for proteins involved in immune regulation, transcription and translation regulation, and apoptosis. Understanding these mechanisms may lead to the design and development of treatments that target tumorigenic cells.