Fig. 4 | Laboratory Investigation

Fig. 4

From: ARHGEF39 promotes tumor progression via activation of Rac1/P38 MAPK/ATF2 signaling and predicts poor prognosis in non-small cell lung cancer patients

Fig. 4

ARHGEF39 (A39) facilitated phosphorylation of P38-ATF2 by activating Rac1. a A549 cells transfected with empty vector or A39 cDNA were subjected to active Rac1, RhoA, RhoC, and Cdc42 pull-down assays. The amount of active or total Rac1, RhoA, RhoC, and Cdc42 are shown, respectively. b Transfection with a plasmid encoding Rac1 (T17N) attenuated the increase of active Rac1, as well as the levels of p-P38 and p-ATF2, induced by A39 overexpression. Transfection with a plasmid encoding Rac1 (Q61L) restored the decrease of active Rac1, as well as the levels of p-P38 and p-ATF2, caused by A39 RNAi. In MTT assays (c), colony formation assays (d, g), wound healing assays (f, i), and Matrigel assays (e, h), the increase in cell proliferation, migration, and invasion, induced by A39 overexpression, was abolished by transfection with Rac1 (T17N), whereas the inhibition of cell proliferation, migration and invasion, caused by A39 RNAi, was restored following transfection with Rac1 (Q61L). Data are shown as the mean ± SD from three independent experiments. *P < 0.05, **P < 0.01; scale bar = 50 μm

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