DCLK1 induces a pro-tumorigenic phenotype to drive gastric cancer progression

Menée in vitro et à l'aide de xénogreffes sur des modèles murins, cette étude met en évidence un mécanisme par lequel la kinase DCLK1 favorise la progression du phénotype des cellules gastriques cancéreuses vers un phénotype pro-invasif et pro-métastatique

Résumé en anglais

Doublecortin-like kinase 1 (DCLK1) is a proposed driver of gastric cancer (GC) that phosphorylates serine and threonine residues. Here, we showed that the kinase activity of DCLK1 orchestrated cancer cell–intrinsic and–extrinsic processes that led to pro-invasive and pro-metastatic reprogramming of GC cells. Inhibition of the kinase activity of DCLK1 reduced the growth of subcutaneous xenograft tumors formed from MKN1 human gastric carcinoma cells in mice and decreased the abundance of the stromal markers