Objectives: The tests conducted were intended to analyze the concentration of p53 protein and anti-p53 autoantibodies in serum of women with ovarian tumours.
Material And Methods: The study included patients with diagnosed ovarian cancer: Cystadenoma serosum or Cystadenocarcinoma papillare serosum at IIIc stage (including 10 women who had G1, 14 women who had G2 and 30 women who had G3 staging). Concentrations of parameters were measured by ELISA.
Results: The analysis of the obtained results showed statistical significance between the concentration of p53 protein depending on the degree of differentiation of G1 and G3 (p < 0.001) and anti-p53 autoantibodies depending on the degree of differentiation of G1 and G2 (p < 0.05) as well as G2 and G3 (p < 0.01). In addition, the determined p53/anti-p53 autoantibodies ratio was only significant between G1 and G2 (p < 0.05), as was the assessment of the percentage of the tested parameters in the immune complex.
Conclusions: Immune system disorders involving the p53 protein and anti-p53 autoantibodies may be one of the immune mechanisms involved in the pathogenesis of ovarian serous cancer.
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http://dx.doi.org/10.5603/GP.a2020.0123 | DOI Listing |
In p53-deficient cancers, targeting cholesterol metabolism has emerged as a promising therapeutic approach, given that p53 loss dysregulates sterol regulatory element-binding protein 2 (SREBP-2) pathways, thereby enhancing cholesterol biosynthesis. While cholesterol synthesis inhibitors such as statins have shown initial success, their efficacy is often compromised by the development of acquired resistance. Consequently, new strategies are being explored to disrupt cholesterol homeostasis more comprehensively by inhibiting its synthesis and intracellular transport.
View Article and Find Full Text PDFFood Sci Nutr
January 2025
Agricultural Extension Directorate, MAAR Damascus Syria.
Coumarins, a group of naturally occurring compounds, have been reported to demonstrate anticancer potential. These substances, distinguished by their combined benzene and α-pyrone rings, have been demonstrated to impact multiple cellular mechanisms essential for the initiation and advancement of cancer. These agents work in different ways that prevent different tumor cells from growing, spreading, and increasing.
View Article and Find Full Text PDFToxicol Res (Camb)
January 2025
Yunnan Provincial Key Laboratory of Public Health and Biosafety and School of Public Health, Kunming Medical University, No. 1168 Chunrongxi Road, Chenggong, Kunming, Yunnan 650500, China.
This study explores the role of Argonaute 2 (AGO2) in the induction of apoptosis by arsenic in 16HBE cells and investigates the association between AGO2 expression and arsenic exposure in a human population. By silencing AGO2 with siRNA, we examined its impact on cell viability and apoptosis using CCK-8, HO-PI, and JC-1 assays, complemented by qRT-PCR and Western blot analyses for gene and protein expressions. Our findings revealed a significant correlation between AGO2 expression and levels of exposure to inorganic arsenic (iAs), which was more pronounced than with other arsenic forms such as monomethylarsonic (MMA) and dimethylarsinic acids (DMA).
View Article and Find Full Text PDFHere, we have discussed the molecular mechanisms of p53-responsive microRNAs dysregulation in response to genotoxic stress in diffuse large B-cell lymphoma (DLBCL) patients. The role of micro ribonucleic acids (microRNAs) in p53-signaling cellular stress has been studied. MicroRNAs are the small non-coding RNAs, which regulate genes expression at post-transcriptional level.
View Article and Find Full Text PDFToxicol Res
January 2025
Department of Pharmacology, College of Medicine, Chungnam National University, 266, Munhwa-ro, Jung-gu, Daejeon, 35015 Republic of Korea.
Over the last decade, the functions of PHD finger protein 20 (PHF20) in several signaling processes have been studied, including those of protein kinase B (PKB)-mediated phosphorylation, p53 regulation, muscle differentiation, and histone modification including histone H3 lysine 4 (H3K4) methylation. One PHF20 human mutation lacks the first nonspecific lethal complex of the component that binds to H3K4me2 to facilitate cancer cell survival. In carcinoma cells, PHF20 expression is regulated by PKB; PHF20 becomes phosphorylated when DNA is damaged, thus inhibiting the p53 activity that maintains cancer cell survival.
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