Pancreatic DCLK1 marks quiescent but oncogenic progenitors: a possible link to neuroendocrine tumors
Doublecortin-like kinase 1 (DCLK1) is a microtubule-associated protein that plays key roles in the regulation of neural cell differentiation, migration, and apoptosis during embryonic development (1,2). Accumulating evidence suggests that DCLK1 is a marker of intestinal and pancreatic stem cells and cancer stem cells; thus, it is attracting attention from both gastroenterologists and oncologists (3-6). The function of DCLK1 is not fully understood; however, at minimum, we know that this kinase induces epithelial-mesenchymal transition (EMT), which supports the stemness of normal and neoplastic stem cells. Regarding mechanism of the DCLK1-induced EMT, involvement of specific microRNA-dependent upregulation of c-MYC, KRAS, and Notch1 expressions was demonstrated in pancreatic and colon cancer cells (7,8). Furthermore, a recent study has strengthened the evidence by shedding light on upregulation the EMT regulator SLUG by DCLK1 that resulted in increased cell migration ability (9).