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. 2024 Sep 9;14(15):5778–5792. doi: 10.7150/thno.95141

Figure 2.

Figure 2

TGFBI induction by HIF1α in GSCs under hypoxia. (A) IHC staining of TGFBI, HIF1α, and SOX2 in the same human high- and low-expression GBM tissues. Scale bars: 40 μm (B) IHC staining demonstrating the association between TGFBI and SOX2 proteins in human gliomas. n = 58 (C) IHC staining demonstrating the association between TGFBI and CD133 proteins in human gliomas. n = 58 (D) IF staining of TGFBI and two stem cell-associated markers (SOX2, CD133) in T387 GSCs. Also shown is the quantification of the relative intensity of fluorescence of T387 and T3691 GSCs (right, n = 5). (E) IB of TGFBI, SOX2, OLIG2, and GFAP proteins in the indicated GSCs and differentiated GSCs (DGS). (F) IB of TGFBI, HIF1α, and HIF2α in matched GSCs cultured under standard (21% O2) or hypoxic (1% O2) conditions for 24 hours. (G) IB of TGFBI protein expression in the GSCs transduced with shCONT or shHIF1α and (H) shHIF2α under hypoxia. (I) qRT-PCR analysis showing mRNA expression of TGFBI and HIF1α in GSCs transduced with shCONT or shHIF1α. (J) ChIP analyses showing HIF1α binding to the TGFBI promoter in GSCs under hypoxia. Data are presented as the mean ± SD. **P <0.01; ***P < 0.001; ****P < 0.0001.