| First Author | Nishide K | Year | 2009 |
| Journal | PLoS One | Volume | 4 |
| Issue | 8 | Pages | e6869 |
| PubMed ID | 19718438 | Mgi Jnum | J:152390 |
| Mgi Id | MGI:4358637 | Doi | 10.1371/journal.pone.0006869 |
| Citation | Nishide K, et al. (2009) Glioblastoma formation from cell population depleted of Prominin1-expressing cells. PLoS One 4(8):e6869 |
| abstractText | Prominin1 (Prom1, also known as CD133 in human) has been widely used as a marker for cancer stem cells (CSCs), which self-renew and are tumorigenic, in malignant tumors including glioblastoma multiforme (GBM). However, there is other evidence showing that Prom1-negative cancer cells also form tumors in vivo. Thus it remains controversial whether Prom1 is a bona fide marker for CSCs. To verify if Prom1-expressing cells are essential for tumorigenesis, we established a mouse line, whose Prom1-expressing cells can be eliminated conditionally by a Cre-inducible DTA gene on the Prom1 locus together with a tamoxifen-inducible CreER(TM), and generated glioma-initiating cells (GICs-LD) by overexpressing both the SV40 Large T antigen and an oncogenic H-Ras(L61) in neural stem cells of the mouse line. We show here that the tamoxifen-treated GICs-LD (GICs-DTA) form tumor-spheres in culture and transplantable GBM in vivo. Thus, our studies demonstrate that Prom1-expressing cells are dispensable for gliomagenesis in this mouse model. |
