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. 2012 Jun 4;1(6):e12. doi: 10.1038/oncsis.2012.12

Figure 4.

Figure 4

Targeting the AKT/cyclin D1/Cdk4 pathway for suppression of radioresistance of 82FR-31NR cells. (a) Western blotting of CD133, P-AKT Ser473, AKT, phosphorylated-p70S6K-Threonine389 (P-P70S6K-Thr389), P70S6K, phosphorylated-S6-Serine240/Serine244 (P-S6-Ser240/244), S6 and β-actin in 0FR and 82FR-31NR cells with rapamycin or API-2. (b) Survival curves of 82FR-31NR cells (open circle), 82FR-31NR cells with API-2 (closed square), 82FR-31NR cells with Cdk4-I (closed triangle), 82FR-31NR cells with rapamycin (closed diamond) of HepG2 on the left and those of A172 on the right, after irradiation. Asterisks indicate significant radioresistance in 82FR-31NR cells with each drug compared with 82FR-31NR cells without drug. (c) Annexin V staining in 82FR-31NR cells. Asterisks indicate significant increase of Annexin V positive cells by treatment with drugs in 82FR-31NR cells in comparison with non-treated cells. (d) Cell growth in 82FR-31NR cells with 2 Gy of FR (closed circle), 82FR-31NR with FR plus API-2 (closed square), non-irradiated 82FR-31NR cells (open circle) and 82FR-31NR with API-2 (open square). Cells were treated with 20 μℳ of API-2 for 24 h once a week. (e) Cell growth in 82FR-31NR cells with 2 Gy of FR (closed circle), 82FR-31NR with FR plus Cdk4-I (closed triangle), non-irradiated 82FR-31NR cells (open circle) and 82FR-31NR with Cdk4-I (open triangle). Cells were treated with 1.9 μℳ of the Cdk4-I for 24 h once a week.