LAUSR

We do not intend to analyze here the meaning of the title of the article “Could We Address the Interplay Between CD133, Wnt/b-Catenin, and TERT Signaling Pathways as a Potential Target for Glioblastoma Therapy?” by Behrooz and Syahir published recently in Frontiers in Oncology [issue April 1, 2021]. Yet, it is important to mention that essential data regarding the biology of prominin-1 (prom1, a.k.a. CD133) are missing and the work of others is mistakenly described. We here provide these quotations to guide the reader to the literature pertinent to the question raised. Targeting prominin-1-expressing cells in relation to signaling cascades for cancer therapy has indeed been the concern of many over the past decade. To fully apprehend the clinical potential of targeting strategies, it is important to provide the complete and accurate account of the biology of prominin-1. Initially identified as a marker for plasma membrane protrusions in mouse embryonic neuroepithelial cells, the primary neural stem cells (1), prominin-1 has been used to identify and purify murine stem cells from the adult subventricular zone along the lateral ventricle walls, hippocampal dentate gyrus, and the postnatal cerebellum, which has important implications for the comprehension of cerebellar development and the origins of medulloblastoma (2–5). Its human homolog (6) was identified on a subpopulation of CD34 hematopoietic stem cells (7) and characterized from retinoblastoma cell lines (8). Human neural precursors were shown to harbor prominin-1 (9), which was later used to identify and purify brain tumor stem cells (10). Since then, prominin-1 has been considered as a prominent marker associated with tumor development in the field [see the review (11) and references therein]. An interconnection between prominin-1 and canonical Wnt pathway was initially suspected in melanoma cells several years ago (12). The downregulation of prominin-1 prevented the nuclear localization of b-catenin and reduced Wnt signaling through TCF/LEF transcription factor (13). Yet, the Wnt/b-catenin pathway could still be activated by its physiological ligands