Expression data of murine capillary endothelial cells after MICAL2 gene knock-down by means of shRNA-expressing lentiviral vectors.

Molecules interacting with CasL 2 (MICAL2) belongs to a three-member family of multi-domain flavoprotein monooxygenase enzymes that catalyze actin oxidation-reduction reactions destabilizing F-actin in cytoskeletal dynamics. MICAL2 is over-expressed, being a negative prognostic factor, in aggressive gastric, kidney, prostate, bladder, breast and endometrial human cancer. MICAL2 is expressed in cancer-associated neo-angiogenic capillaries. The study of MICAL2 knock-down in endothelial cells shed light on the transcriptional impact of the gene on endothelial cell biology. To explore the transcriptional impact of the lack of Mical2 in endothelial cells, we performed genome-wide expression profiling of Mical2 knock-down SVEC4-10 (ATTC CRL-2181) cells (M2KD). Reference cells were: Mical3 knock-down (M3KD), obtained with same strategy; untreated SVEC4-10 cells ((WT), and cells transduced with insert-free viral vector (empty). Gene expression profiling was performed to identify transcripts modulated by the absence of the F-actin modifying redox enzyme MICAL2 that affects the pro-angiogenic and therefore pro-cancer activity of endothelial cells.