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. Author manuscript; available in PMC: 2019 Oct 29.
Published in final edited form as: Clin Cancer Res. 2017 Sep 14;23(22):7047–7058. doi: 10.1158/1078-0432.CCR-17-0077

Figure 4. hIFNβ suppresses tumor growth through Chk1 mediated S phase arrest followed by apoptosis:

Figure 4.

(A) Heat map and box and whisker plot showing relative transcriptional expressional level of IFNAR1 and IFNAR2 compared to EGFR and VEGFA analyzed from TCGA-GBM RNA-Seq database (n=166 GBM patients). (B) RT-PCR analysis of IFNAR1/2 in cDNA extracts from GBM lines (C) Cell viability of GBM lines 72h post-treatment with hIFNβ (100ng/ml). (D) Flow cytometry analysis of GBM4 cells treated with hIFNβ for 120h, followed by a 1h BrdU pulse. (E) The comparison of the number of GBM4 cells 24h and 48h post-treatment of hIFNβ (100ng/ml). (F) Western blot analysis of PARP and cleaved-PARP (c-PARP) from GBM4 cells in response to hIFNβ (100ng/ml) treatment. (G) Western blot analysis of GBM lysates to detect phosphorylated STAT1 (Tyr701) and STAT1 overexpression induced 24h post-hIFNβ (100ng/ml) treatment. (I) Western blot analysis of lysates from GBM4 cells treated with hIFNβ (100ng/ml) for 24, 48, and 72hrs showing phosphorylation status of STAT1 (Tyr701), p38 (T189/Y182), Chk1 (S345), and Akt (S473).