Figure 4.

DDX39B promotes cellular clonogenicity and is elevated in diverse cancers.

HeLa cells were transfected with (A) pEGFP-C1 vector or pEGFP-DDX39B construct or (B) control siRNA or siDDX39B-1. Colony forming capacity was measured by staining the colonies with crystal violet, 10 days after transfection. Experiments were performed in triplicates and representative images are provided here. Colony numbers were counted using ImageJ software and the values in the graph represent the mean of triplicates and the error bars represent the standard deviations. Statistical significance was assessed using two-tailed t-test. ** indicates P-value <0.01. (C) DDX39B is significantly upregulated in diverse cancers. Differential expression of DDX39B in different cancer types is shown as log2 fold changes (represented by green bars), with each cancer type abbreviated in the X-axis. The yellow line shows the distribution of – Log10 FDR values (False Discovery Rates; P-values corrected for multiple testing for each cancer type by Benjamini-Hochberg method), with the dots representing the value for the corresponding cancer type. The horizontal dotted line represents the FDR cut-off of 0.05, indicating statistical significance. The numbers given in the parenthesis provide the number of patients for which the expression data for each cancer type was available. KICH; kidney chromophobe, PRAD; prostate adenocarcinoma, LIHC; liver hepatocellular carcinoma, HNSC; head and neck squamous cell carcinoma, LUAD; lung adenocarcinoma, THCA; thyroid carcinoma, UCEC; uterine corpus endometrial carcinoma, STAD; stomach adenocarcinoma, CESC; cervical squamous cell carcinoma and endocervical adenocarcinoma, PAAD; pancreatic adenocarcinoma, BLCA; bladder urothelial carcinoma, KIRC; kidney renal clear cell carcinoma, LUSC; lung squamous cell carcinoma, BRCA; breast invasive carcinoma, ESCA; esophageal carcinoma, KIRP; kidney renal papillary cell carcinoma.