TGF-β受体抑制剂能靶向抑制CD44high/Id1high表型的成胶质瘤起始细胞

饶冠华

TGF-β Receptor Inhibitors Target the CD44high/Id1high Glioma-Initiating Cell Population in Human Glioblastoma
1 Q& d) o2 v' `' x% M8 @7 Z0 [J. Anido, A. Sáez-Borderías, A. Gonzàlez-Juncà, L. Rodón, G. Folch, M.A. Carmona, R.M. Prieto-Sánchez, I. Barba, E. Martínez-Sáez, L. Prudkin, I. Cuartas, C. Raventós, F. Martínez-Ricarte, M.A. Poca, D. García-Dorado, M.M. Lahn, J.M. Yingling, J. Rodón, J. Sahuquillo, J. Baselga, and J. Seoane
, S0 J' }. G# X' h" j+ jSee also Edwards and Fine8 ?% S0 I4 `+ G# _* x! W
    . }( S9 z2 c- }, U/ ~3 u1 S; k
* F& k0 X  K4 S3 [
Glioblastoma mutliforme (GBM) is one of the most aggressive and recalcitrant tumors, and glioma-initiating cells (GICs) are responsible for therapeutic failures. Still, not many therapeutic approaches have been described to target GICs. Through the study of patient-derived tumor specimens, it has been observed that the inhibition of the TGF-β pathway targets a cell population characterized by high expression of CD44 and Id1, which is enriched for GICs. The depletion of the CD44high/Id1high GIC population by TGF-β inhibitors prevents tumor initiation and recurrence. This work shows that Id1 and Id3 are therapeutic targets against GICs and GBM, and that combined CD44 and Id1 expression confers poor prognosis in patients. Furthermore, the results have clear implications on the clinical development of TGF-β inhibitors as compounds targeting GICs.1 ~4 V/ W6 z( x# b