Fig. 4: PI3K-mediated phosphorylation of AKT and EGFR by LRIG2 mediates the growth-inhibitory effects of LRIG2. | Oncogenesis

Fig. 4: PI3K-mediated phosphorylation of AKT and EGFR by LRIG2 mediates the growth-inhibitory effects of LRIG2.

From: LRIG2 is a growth suppressor of Hec-1A and Ishikawa endometrial adenocarcinoma cells by regulating PI3K/AKT- and EGFR-mediated apoptosis and cell-cycle

Fig. 4

a, b LRIG2-overexpressing Hec-1A cells were treated with DMSO (0.1%), LY294002 (30 µM), gefitinib (10 µM), U0126 (10 µM), or SP600125 (10 µM) for 24 h, and cell viability a and cell proliferation b were assayed. Results are mean ± SEM of three independent experiments performed in triplicates. c, d Hec-1A cells were transfected with control siRNAs, AKT-specific siRNA, or EGFR-specific siRNAs for 24 h, followed by LRIG2 overexpression for additional 24 h. Then, cell viability c and cell proliferation d were determined. e Hec-1A cells were transfected with siRNA #1 for LRIG2. Representative immunoblots and quantified results of three independent experiments for the indicated kinases are shown. f Cells presented in a were used. Representative immunoblot results and quantified data (mean ± SEM) from three independent experiments are shown. Asterisks and different letters indicate statistically significant values (p < 0.05)

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