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. 2017 Jul 28;20(2):236–248. doi: 10.1093/neuonc/nox142

Fig. 3.

Fig. 3

Secondary GSCs represent a stable and cell intrinsic TMZ resistance phenotype, coupled with a loss of mesenchymal characteristics. (A, B) TMZ resistance of GSCs is maintained in sphere culture (MTS viability assay, see text). MTS assay after TMZ treatment in 2 SGSC lines (1123IC8R, 1123IC7R) from TMZ-unresponsive tumors and 2 SGSC lines from control tumors (1123IC12S, 1123IC13S) (N = 3; 100% = no TMZ). ****P < 0.0001. (C–E) TGM2 downregulation and Nestin induction in TMZ resistant phenotype were observed in vitro after isolation of SGSCs from xenograft tumors, at the mRNA level tested by qPCR (C, D) (1 = average mRNA expression in TMZ-sensitive cell lines), and at the protein level by western blot (E). ****P < 0.0001; **P < 0.01 (N = 3). (F–H) Immunostaining of mesenchymal control (PT1123ICxS) and TMZ-treated (PT1123ICxR) intracranial tumors confirmed the variability in protein expression, a trend toward a decrease in mesenchymal markers TGM2 and CD44, and an upregulation of Nestin expression after acquisition of resistance to TMZ (objective 20x).