Peroxiredoxins are thiol-specific antioxidant proteins whose expression is elevated in several cancers. We compared the expression and function of Prdx1 and Prdx6 between the MCF-7 mammary adenocarcinoma cell line and the noncancerous MCF-10A cell line. We found elevated Prdx1 expression in MCF-7 cells and comparable expression of Prdx6. Suppression of Prdx1 and/or Prdx6 resulted in a modest increase in peroxide-induced cytotoxicity of MCF-7 cells, and a dramatic increase in MCF-10A cytotoxicity with and without hydrogen peroxide treatment. Our data confirm a cytoprotective role for peroxiredoxins and suggest a synergistic role for Prdx1 and Prdx6 in MCF-10A cells.
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http://dx.doi.org/10.3109/07357907.2011.629382 | DOI Listing |
J Transl Med
January 2025
Medical College of YiChun University, Xuefu Road No 576, Yichun, 336000, Jiangxi, People's Republic of China.
Background: Artificial sweeteners (AS) have been widely utilized in the food, beverage, and pharmaceutical industries for decades. While numerous publications have suggested a potential link between AS and diseases, particularly cancer, controversy still surrounds this issue. This study aims to investigate the association between AS consumption and cancer risk.
View Article and Find Full Text PDFRespir Res
January 2025
Department of Obstetrics and Gynecology, C.S. Mott Center for Human Growth and Development, School of Medicine, Wayne State University, 275 E Hancock St, Rm 195, Detroit, MI, 48201, USA.
Current fetal alcohol spectrum disorders (FASD) studies primarily focus on alcohol's actions on the fetal brain although respiratory infections are a leading cause of morbidity/mortality in newborns. The limited studies examining the pulmonary adaptations in FASD demonstrate decreased surfactant protein A and alveolar macrophage phagocytosis, impaired differentiation, and increased risk of Group B streptococcal pneumonia with no study examining sexual dimorphism in adaptations. We hypothesized that developmental alcohol exposure in pregnancy will lead to sexually dimorphic fetal lung morphological and immune adaptations.
View Article and Find Full Text PDFHum Genomics
January 2025
Population Health Program, QIMR Berghofer Medical Research Institute, Herston, QLD, 4006, Australia.
Background: TP53 variant classification benefits from the availability of large-scale functional data for missense variants generated using cDNA-based assays. However, absence of comprehensive splicing assay data for TP53 confounds the classification of the subset of predicted missense and synonymous variants that are also predicted to alter splicing. Our study aimed to generate and apply splicing assay data for a prioritised group of 59 TP53 predicted missense or synonymous variants that are also predicted to affect splicing by either SpliceAI or MaxEntScan.
View Article and Find Full Text PDFEur J Med Res
January 2025
Department of Neurosurgery, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, No 17 Panjiayuan Nanli, Chaoyang District, Beijing, 100021, People's Republic of China.
Objective: This study aimed to evaluate CTF1 expression in glioma, its relationship to patient prognosis and the tumor immune microenvironment, and effects on glioma phenotypes to identify a new therapeutic target for treating glioma precisely.
Methods: We initially assessed the expression of CTF1, a member of the IL-6 family, in glioma, using bioinformatics tools and publicly available databases. Furthermore, we examined the correlation between CTF1 expression and tumor prognosis, DNA methylation patterns, m6A-related genes, potential biological functions, the immune microenvironment, and genes associated with immune checkpoints.
J Cardiothorac Surg
January 2025
Department of Respiratory and Critical Care Medicine, Datian County General Hospital, 180 Xueshan North Road, Datian County, 366100, China.
Background: Lung adenocarcinoma is the most common form of lung cancer and one of the most life-threatening malignant tumors. Ferroptosis is an iron-dependent regulatory cell death pathway that is crucial for tumor growth. SNX30 is a key regulatory factor in cardiac development; however, its regulatory mechanism and role in inducing ferroptosis in lung adenocarcinoma remain unclear.
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