p53 inhibition triggers MM cell growth inhibition. (A) MM.1S infected with control (left panel) or p53 shRNA (B10, right panel) was subjected to propidium iodide staining and cell-cycle analysis using flow cytometry. (B) MM.1S cells (left panel) and H929 cells (right panel) were infected with lentiviral Sc or p53 shRNA/siRNA, respectively. (C, D) H929 cells were transfected with Sc or p53 siRNA. Whole cell lysates and nuclear extracts were subjected to western blot (C) and EMSA (D), respectively. Densitometric analysis was performed on E2F EMSA. (E) p53 was knocked down in MM.1S cells (left panel) and H929 (right panel) using shRNA and siRNA, respectively. (F) MM.1S and H929 cells were transfected with p53 or Myc siRNA. mRNAs from transfectants were extracted and subjected to real-time qPCR for c-Myc or p53; purple, MM.1S Sc shRNA; blue, MM.1S c-Myc shRNA; red, H929 Sc siRNA; green, H929 c-Myc siRNA. (G) Normalized (average reads per million) c-MYC, ac-H3K27, or tri-methylated H3K4 chromatin immunoprecipitation-sequencing tag counts around (±5 kb) the transcription start site of IKZF1. (H) H929 cells were transfected with Sc or c-Myc siRNA. Extracted mRNA was subjected to qPCR for IKZF1/3. (I) MM.1S cells were infected with Luc or TP53RK shRNA. (J) p53-deficient (KMS-11) MM cells were transfected with Sc or TP53RK siRNA. Cell growth was assessed by MTT assay after 72-hour incubation.