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Fig. 4 | Infectious Agents and Cancer

Fig. 4

From: HIV-1 matrix protein p17 and its variants promote human triple negative breast cancer cell aggressiveness

Fig. 4

Role of MEK/ERK signaling pathway in migration induced by refp17 and vp17s. MDA-MB 231 cells were serum starved for 24 h in the presence or absence of the PI3K/Akt inhibitor LY294002 (20 μM), the Jak/STAT inhibitor AG-490 (20 μM), or the MEK/ERK1/2 inhibitor PD98059 (10 μM). a Confluent cell monolayers were serum starved for 24 h and then scratched with a 200 μl pipette tip. Cells were then incubated for 6 h in the absence (NT) or in the presence of 10 ng/ml of refp17 or vp17s. Images are representative of three independent experiments with similar results (original magnification 10×). Statistical analysis was performed by one-way ANOVA and the Bonferroni’s post-test was used to compare data (*** p < 0.001). b MDA-MB 231 cells were stimulated or not (NT) for 30 min with 200 ng/ml of refp17 or vp17s and then lysed. Equal amounts of total cellular extracts were analyzed for expression of pERK1/2 or ERK1/2 by western blot analysis using mAbs to pERK1/2 (Thr202, Tyr204) or ERK1/2 as specific reagents. Phosphorylation of ERK1/2 was verified by densiometric analysis and plotting of the pERK1/2/ERK1/2. Upper panel, Blots from one representative experiment of three with similar results are shown. Lower panel, Values reported for ERK1/2 are the mean ± SD of three independent experiments. Statistical analysis was performed by one-way ANOVA, and the Bonferroni post-test was used to compare data

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