SUM-149PT cells are known to exhibit the Tandem Duplicator Phenotype of genomic instability. This phenotype results in small tandem duplications that occur throughout the genome and is distinct from the mechanism that results in focal areas of gene amplification that activate oncogenes such as HER2, FGFR2/3, CCND1 etc. Thus, the “functional oncogene signature” shown below which we define as those genes that are copy number amplified, overexpressed at the message level and were hits in our shRNA screen does not reveal any particularly interesting oncogenes. Indeed, only two of these genes have gene ranker scores greater than 1. Below is the list of “functional oncogenes” in SUM-149 cells.
| ids | quantrank | Gene ranker >1 |
| LIN9 | 885 | |
| PDLIM3 | 527 | |
| RPS6 | 941 | yes |
| NAT10 | 240 | |
| EIF3M | 478 | |
| ELP4 | 418 | yes |
| TRIM44 | 954 |
When we examine the data in another way, by looking at the genes that are amplified and overexpressed in SUM-149 cells and make the COSMIC cancer gene census, we find the following list of genes: H3F3A, PSIP1, NFIB, WT1, EXT2, and none of these genes were hits in the functional screen. We conclude from this analysis that gene amplification and overexpression is not an important mechanism for oncogene activation in these cells.
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