Fig. 7: CUL4A increases genomic instability and enhances subsequent malignant transformation. | Oncogene

Fig. 7: CUL4A increases genomic instability and enhances subsequent malignant transformation.

From: CRL4ADTL degrades DNA-PKcs to modulate NHEJ repair and induce genomic instability and subsequent malignant transformation

Fig. 7

(A) Hoechst staining of Cre;LSL-Cul4a and Cre;LSL-Dtl MEF nuclei to show multinucleated cells. (B) Chromosome morphology analysis showed the effect of CUL4A and DTL on the chromosome structure in HPDE6-C7 cells. (C, D) Fourteen days after IR, MTT, and colony formation assays were used to examine the effect of CUL4A and DTL on the proliferative potential of HPDE6-C7 cells. (E) Histogram showing the statistical analysis of the protein expression levels of CUL4A, DNA-PKcs, and γ-H2AX in pancreatic tissue (N), chronic pancreatitis tissue (CP), and intraductal papillary mucinous neoplasm (IPMN) tissue, as detected by Western blotting. (F, G) Correlation analysis between CUL4A and DNA-PKcs or γ-H2AX in chronic pancreatitis tissues or intraductal papillary mucinous neoplasm tissues, respectively. (H) Immunohistochemical analysis of CUL4A, DNA-PKcs, and γ-H2AX protein expression levels in intestinal metaplasias of the gastric mucosa. (I) Correlation analysis between CUL4A and DNA-PKcs or γ-H2AX in intestinal metaplasias of the gastric mucosa. * p < 0.05 and ** p < 0.01 based on Student’s t-test in C and E and correlation test in F, G, and I. The data are presented as the means ± SDs of three (A) independent experiments. The scale bars indicate 25 μm in A.

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