Identification of cancer‐specific genes and pathways in rat liver tumor cells after human chromosome 11‐mediated suppression of tumorigenicity

Human chromosome 11p11.2 suppresses the tumorigenic potential and alters the cellular behavior of GN6TF rat liver tumor cells secondary to expression of the Syt13 liver tumor suppressor gene resulting in normalized GN6TF‐11neo CX4 cells. Affymetrix GeneChip Rat Genome 2.0 Arrays were used to assess gene expression patterns in suppressed GN6TF‐11neo CX4 cells, the parental GN6TF tumor cells, CX4 cells after RNAi‐mediated knockdown of Syt13 (i12 cells), and scrambled control cells (s1 cells). Pathway analysis was performed using the Database for Annotation, Visualization and Integrated Discovery (DAVID) in conjunction with the Kyoto Encyclopedia of Genes and Genomes (KEGG). 436 genes were 2‐fold upregulated and 351 genes were 2‐fold downregulated in CX4 versus GN6TF cells. Multiple pathways associated with focal adhesion, cell‐cell interaction, and cell‐ECM interaction were found to be overrepresented among upregulated genes in the CX4 cell line. 77 genes were 2‐fold upregulated and 41 genes were 2‐fold downregulated in CX4 cells versus i12 cells, including genes associated with focal adhesion and cell signaling. 61 genes were 2‐fold upregulated and 101 genes were 2‐fold downregulated in i12 cells versus s1 cells. Mining the intersection of the gene lists resulting from this analysis should identify cancer‐specific genes and pathways that are critical to expression of tumorigenic potential in this model system.