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. 2018 Jun 4;13(6):e0198364. doi: 10.1371/journal.pone.0198364

Fig 4. Dermatan sulfate epimerase 1 (DSE) modulates heparin-binding EGF-like growth factor (HB-EGF)/ErbB signaling in glioma cells.

Fig 4

(A) Knockdown of DSE suppressed HB-EGF-induced downstream signaling. U118 transfectants were treated without (−)/with (+) HB-EGF for 5 and 15 min. Phosphorylation levels of ERK, AKT, total ERK, and AKT were measured by western blotting. Signals were quantified by Image J, and represented as means ± SD from three independent experiments. **P < 0.01 (B) Knockdown of DSE suppressed epidermal growth factor receptor (EGFR) and ErbB2 activation. The protein expression and phosphorylation of EGFR and ErbB2 were analyzed by western blotting with the indicated antibodies. Actin was used as a loading control. (C) Overexpression of DSE enhanced HB-EGF-induced signaling. GL261 transfectants were treated without (−)/with (+) HB-EGF or EGF. Cell lysates were analyzed by western blotting with various antibodies, as indicated. (D) The correlation of DSE expression with EGFR, ERBB2, and ERBB4. Expression of DSE and ERBB2 were positively correlated in glioma patients. Data were analyzed using the REMBRANDT database (http://www.betastasis.com/glioma/rembrandt/).