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http://dx.doi.org/10.1055/s-0028-1099941 | DOI Listing |
Front Cell Infect Microbiol
March 2024
Institute of Virology, Saarland University Medical Center, Homburg, Germany.
Aging (Albany NY)
March 2023
School of Basic Medical Sciences, Anhui Medical University, Hefei 230032, China.
Background: Matrix metalloproteinase-13 (MMP13) is a member of the endopeptidase matrix metalloproteinase family, which is involved in many normal physiological processes and even tumorigenesis. However, its co-carcinogenic signature in different cancers is not fully understood.
Methods: In this study, we first analyzed the expression of MMP13 in pan-cancer and its association with prognosis, immune infiltration, and cancer-related signaling pathways through integrated bioinformatics.
Toxicol Appl Pharmacol
November 2022
Department of Pharmaceutical Sciences, University of New Mexico Health Sciences Center, 1 University of New Mexico, Albuquerque, NM 87131, USA. Electronic address:
Arsenite interferes with DNA repair protein function resulting in the retention of UV-induced DNA damage. Accumulated DNA damage promotes replication stress which is bypassed by DNA damage tolerance pathways such as translesion synthesis (TLS). Rad18 is an essential factor in initiating TLS through PCNA monoubiquitination and contains two functionally and structurally distinct zinc fingers that are potential targets for arsenite binding.
View Article and Find Full Text PDFToxics
January 2022
Institute for Prevention and Occupational Medicine of the German Social Accident Insurance, Institute of the Ruhr-University Bochum (IPA), 44789 Bochum, Germany.
The WHO classified air pollution as a human lung carcinogen and polycyclic aromatic hydrocarbons (PAHs) are components of both indoor (e.g., tobacco smoke and cookstoves) and outdoor (e.
View Article and Find Full Text PDFMol Oncol
March 2022
Institute of Pathology, University of Regensburg, Germany.
Aberrant activation of the phosphoinositide 3-kinase (PI3K)/AKT/mTOR and Ras/mitogen-activated protein kinase (MAPK) pathways is a hallmark of hepatocarcinogenesis. In a subset of hepatocellular carcinomas (HCCs), PI3K/AKT/mTOR signaling dysregulation depends on phosphatidylinositol-4,5-bisphosphate 3-kinase, catalytic subunit alpha (PIK3CA) mutations, while RAS/MAPK activation is partly attributed to promoter methylation of the tumor suppressor Ras association domain-containing protein 1 (RASSF1A). To evaluate a possible cocarcinogenic effect of PIK3CA activation and RASSF1A knockout, plasmids expressing oncogenic forms of PIK3CA (E545K or H1047R mutants) were delivered to the liver of RASSF1A knockout and wild-type mice by hydrodynamic tail vein injection combined with sleeping beauty-mediated somatic integration.
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