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. 2018 Jan 12;9(16):12982–12994. doi: 10.18632/oncotarget.24204

Figure 5. Inhibition of PI3K/Akt totally blocked the promotion of HC11 proliferation induced by OA.

Figure 5

(A) Effect of Wortmannin (WT), an inhibitor of PI3K, on the proliferation of HC11 after a 4-day incubation was determined by MTT assay. (B) The relative mRNA expression level of Cyclin D1, Cyclin D3, and PCNA in response to 100 μM OA and/or 100 nM WT. (C) Representative immunofluorescence staining of Cyclin D1 and p21 in the presence of 100 μM OA and/or 100 nM WT. Scale bar = 100 μm. (D) Analysis of the relative fluorescence intensity in panel (C). (E) Western blot analysis of p-PI3K, PI3K, p-Akt, Akt, Cyclin D1 and p21 in HC11 after a 4-day culture in the presence of 100 μM OA and/or 100 nM WT. β-actin was used as the loading control. (F) Mean ± SEM of immunoblotting bands of p-PI3K/PI3K, p-Akt/Akt, Cyclin D1, and p21, and the intensities of the bands were expressed as the arbitrary units. **P < 0.01 versus the Control group, ##P < 0.01 versus the 100 μM OA group.