In vivo transcriptome profiling of control and GANAB-KD UMUC3 bladder carcinoma cells [scRNA-Seq]

Carcinoma cells achieve malignant progression and therapy resistance through de-differentiation. While differentiation therapy has proven to be highly efficient in acute promyelocytic leukemia, this therapeutic strategy has not been successfully applied in human solid tumors. Here, we identify α-Glucosidase II (GANAB) as a novel driver of bladder cancer de-differentiation using a systemic biology approach and demonstrate its potential to serve as a therapeutic target of solid tumor differentiation therapy. Partial knock-out of GANAB by CRISPR Cas9 differentiates one of the most aggressive bladder carcinoma line into a non-invasive papillary form in vivo and decreases chemotherapy resistance in vitro. As differentiation and de-differentiation program are mostly activated in vivo, we labelled control and GANAB-KD cells with a lentivirus to express a H2B-EGFP localized in the nuclei. After sorting by BD FACS Aria II, cells were lyzed for RNA-sequencing. 2 samples were analyzed, including CTR for control UMUC3, and KD for GANAB-KD UMUC3.