Objective: To evaluate the activity of DNA polbeta promoter on p53 gene in salivary adenoid cystic carcinoma (SACC) cells.
Methods: The luciferase activity was examined and used to evaluate the activity of DNA polbeta promoter on SACC-83 cells. Eukaryotic expression plasmids of p53 gene were constructed and stably transfected into SACC-83 cells. RT-PCR was used to assess the expression of p53 gene. The SACC-83 cells were subjected to the treatments of H2O2, ultraviolet radiation, Bleocin, and affected p53 mRNA and protein level in SACC-83 cells were characterized with RT-PCR and Western blotting.
Results: The result of luciferase activity proved that the activity of DNA polbeta promoter in SACC-83 cells was much higher than that of CMV promoter. The results of RT-PCR suggested that p53 gene with different promoters were all expressed effectively, but the expression efficiency was different. It was greater in DNA polbeta group than in CMV group. After DNA damage, p53 gene expression increased and DNA polbeta promoter could enhance the expression of p53 gene more than CMV promoter. The results of Western blotting indicated that the expression of P53 protein between the two groups did not show any difference.
Conclusion: In SACC cells, the activity of DNA polbeta promoter was increased and DNA polbeta promoter could enhance the expression of p53.
Download full-text PDF |
Source |
---|
Free Radic Biol Med
December 2024
Hematology Institute, School of Medicine, Northwest University, Xian 710069, Shaanxi, China; Deparment of Hematology, Affiliated Hospital of Northwest University & Xian No. 3 Hospital, Xian 710018, Shaanxi, China. Electronic address:
Despite the improvements in outcomes for patients with multiple myeloma (MM) over the past decade, the disease remains incurable, and even those patients who initially respond favorably to induction therapy eventually suffer from relapse. Consequently, there is an urgent need for the development of novel therapeutic agents and strategies to enhance the treatment outcomes for patients with MM. The proteasome inhibitor bortezomib (BTZ) elicits endoplasmic reticulum (ER) stress and oxidative stress in MM cells, subsequent DNA damage, ultimately inducing cell apoptosis.
View Article and Find Full Text PDFEMBO Rep
December 2024
Department of Biochemistry, University of Toronto, Toronto, ON, M5S 1A8, Canada.
Poly(ADP-ribose) polymerase 1 (PARP1) is one of the first responders to DNA damage and plays crucial roles in recruiting DNA repair proteins through its activity - poly(ADP-ribosyl)ation (PARylation). The enrichment of DNA repair proteins at sites of DNA damage has been described as the formation of a biomolecular condensate. However, it remains unclear how exactly PARP1 and PARylation contribute to the formation and organization of DNA repair condensates.
View Article and Find Full Text PDFBase excision repair (BER) maintains genome integrity by fixing oxidized bases that could be formed when reactive oxygen species attack directly on the DNA. We previously reported the importance of a proper coordination at the downstream steps involving gap filling by DNA polymerase (pol) β and subsequent nick sealing by DNA ligase (LIG) 1 or 3α. Yet, how the fidelity of 8-oxoG bypass by polβ affects the efficiency of ligation remains unclear.
View Article and Find Full Text PDFDNA Repair (Amst)
November 2024
Department of Pharmacological Sciences, Stony Brook University School of Medicine, Basic Science Tower 8-140, Stony Brook, New York 11794, USA; Department of Radiation Oncology, Renaissance School of Medicine, Stony Brook University, Stony Brook, New York 11794, USA. Electronic address:
Free radicals produce in DNA a large variety of base and deoxyribose lesions that are corrected by the base excision DNA repair (BER) system. However, the C1'-oxidized abasic residue 2-deoxyribonolactone (dL) traps DNA repair lyases in covalent DNA-protein crosslinks (DPC), including the core BER enzyme DNA polymerase beta (Polβ). Polβ-DPC are rapidly processed in mammalian cells by proteasome-dependent digestion.
View Article and Find Full Text PDFCarcinogenesis
November 2024
Department of Population & Public Health Sciences, USC Keck School of Medicine, University of Southern California, M/C 9603, Los Angeles, CA 90033, United States.
We investigated the interplay among oxidative DNA damage and repair, expression of genes encoding major base excision repair (BER) enzymes and bypass DNA polymerases, and mutagenesis in mammalian cells. Primary mouse embryonic fibroblasts were challenged with oxidative stress induced by methylene blue plus visible light, and formation and repair of DNA damage, changes in gene expression, and mutagenesis were determined at increasing intervals posttreatment (0-192 hours). Significant formation of oxidative DNA damage together with upregulation of Ogg1, Polβ, and Polκ, and no changes in Mutyh and Nudt1 expression were found in treated cells.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!