GSE175415
Next generation sequencing facilitates quantitative analysis of control and NICD overexpression salivary gland imagnal ring tumor transcriptomes
We established a tumor model in which Notch overexpression can induce tumor formation in a transition-zone (TZ) region in the Drosophila salivary gland imagnal ring (ImR). TZ cells are polyploid cells and do not devide during normal development, however, polyploid TZ cells reenter to mitosis and form tumor after Notch induction. Growth and progression of the TZ tumor are fueled by a combination of polyploid mitosis, endoreplication, and depolyploidization. To determine the molecular mechanisms underlying tumor formation in the NICD-induced TZ tumors, we did RNA-seq and compared the transcriptomes between tumor and control. We found the mitosis of the salivary gland ImR tumor was due to the Drosophila Cdc25 homolog String (Stg), a M-phase inducer phosphatase, was significantly upregulated in the tumor sample. Besides, we found DNA damage response genes, also active during meiosis, are upregulated in these tumors and are required for the ploidy reduction division. This study suggests that polyploidy and associated cell-cycle variants are critical for increased tumor cell heterogeneity and genome instability during cancer progression. Overall design: Examination of gene expression from 3 control samples and 3 ImR tumor samples