Figure 5
Figure 5. Epigenetic silencing of both miR-193a and PTEN contributes partially to the activation of CCND1 and MDM2 via the P13K/AKT signal pathway. (A) Relative qRT-PCR quantification of CCND1 level in MNC isolated from 81 AML FAB M2 patients. P = .02. (B) Relative quantification of AML1/ETO and CCND1 mRNA levels in the indicated cell lines. Zn2+ (100μM for 16 hours) were used to increase the AML1/ETO levels in U937 cells. The results represent the average of 3 independent evaluations ± SD. (C) Immunoblot analysis demonstrated the down-regulation of KIT and its downstream effectors as indicated in SKNO-1 (WT, mock, and siA/E; left panels) and U937 (mock and A/E; right panels) cell lines treated with PI3K inhibitor Ly294002 or/and with Zn2+.

Epigenetic silencing of both miR-193a and PTEN contributes partially to the activation of CCND1 and MDM2 via the P13K/AKT signal pathway. (A) Relative qRT-PCR quantification of CCND1 level in MNC isolated from 81 AML FAB M2 patients. P = .02. (B) Relative quantification of AML1/ETO and CCND1 mRNA levels in the indicated cell lines. Zn2+ (100μM for 16 hours) were used to increase the AML1/ETO levels in U937 cells. The results represent the average of 3 independent evaluations ± SD. (C) Immunoblot analysis demonstrated the down-regulation of KIT and its downstream effectors as indicated in SKNO-1 (WT, mock, and siA/E; left panels) and U937 (mock and A/E; right panels) cell lines treated with PI3K inhibitor Ly294002 or/and with Zn2+.

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