A RUNX2-Mediated Epigenetic Regulation of the Survival of p53 Defective Cancer Cells
Fig 1
RUNX2 depletion causes apoptosis in OS cells.
(A) Immunoblotting (I.B.) to examine the levels of RUNX2, p53 and β-actin in hMSCs and human OS cells. Below p53 I.B. are the genotypes of p53 of each cell line. WT, wild type; Null, p53 deletion; MT, mutant. (B) I.B. of RUNX2, cleaved PARP and Tubulin in SAOS2 cells transduced with lentiviruses expressing shLuc, shRUNX2_3 or shRUNX2_4. (C) Propidium iodide staining showing sub-G1 (apoptosis), G1, S, and G2 phases of SAOS2 cells transduced with lentiviruses expressing shLuc, shRUNX2_3 or shRUNX2_4. Numbers below histograms are percentages of phases. (D) Cumulative cell number of SAOS2 cells transduced with lentiviruses expressing shLuc, shRUNX2_3 or shRUNX2_4. (E) A representative image of tumors generated from SAOS2 cells transduced with lentiviruses expressing shLuc, shRUNX2_3 or shRUNX2_4. (F) Weight of tumors generated from SAOS2 cells transduced with lentiviruses expressing shLuc, shRUNX2_3 or shRUNX2_4 in NSG mice. ***, p<0.001; n = 10. (G) Hematoxylin and Eosin staining and Masson’s trichrome staining of SAOS2 tumors. Arrows indicate osteoid formation, the characteristics of OS.