Redox regulation meets metabolism: targeting PRDX2 to prevent hepatocellular carcinoma
PRDX2 acts as a central redox hub linking metabolic dysfunction‐associated steatohepatitis (MASH) to hepatocellular carcinoma (HCC). In normal hepatocytes, PRDX2 maintains redox balance and metabolic homeostasis under oxidative stress. In contrast, during malignant transformation, PRDX2 promotes oncogenic signaling, stemness, and tumor initiation ...
Naroa Goikoetxea‐Usandizaga +2 more
wiley +1 more source
Etoposide induces DNA damage, activating p53‐dependent apoptosis via caspase‐3/7, which cleaves PARP1. Dammarenediol II enhances this apoptotic pathway by suppressing O‐GlcNAc transferase activity, further decreasing O‐GlcNAcylation. The reduction in O‐GlcNAc levels boosts p53‐driven apoptosis and influences the Akt/GSK3β/mTOR signaling pathway ...
Jaehoon Lee +8 more
wiley +1 more source
Biomarkers of basal cell carcinoma resistance to methyl-aminolevulinate photodynamic therapy [PDF]
This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Gilaberte, Yolanda +6 more
core +4 more sources
Correlation of the differential expression of PIK3R1 and its spliced variant, p55α, in pan‐cancer
PIK3R1 undergoes alternative splicing to generate the isoforms, p85α and p55α. By combining large patient datasets with laboratory experiments, we show that PIK3R1 spliced variants shape cancer behavior. While tumors lose the protective p85α isoform, p55α is overexpressed, changes linked to poorer survival and more pronounced in African American ...
Ishita Gupta +10 more
wiley +1 more source
The antagonism between MCT-1 and p53 affects the tumorigenic outcomes
Background MCT-1 oncoprotein accelerates p53 protein degradation via a proteosome pathway. Synergistic promotion of the xenograft tumorigenicity has been demonstrated in circumstance of p53 loss alongside MCT-1 overexpression.
Lin Tai-Du +6 more
doaj +1 more source
Pharmacologically blocking p53-dependent apoptosis protects intestinal stem cells and mice from radiation. [PDF]
Exposure to high levels of ionizing radiation (IR) leads to debilitating and dose-limiting gastrointestinal (GI) toxicity. Using three-dimensional mouse crypt culture, we demonstrated that p53 target PUMA mediates radiation-induced apoptosis via a cell ...
Cramer, Julie M +14 more
core +2 more sources
Tumour–host interactions in Drosophila: mechanisms in the tumour micro‐ and macroenvironment
This review examines how tumour–host crosstalk takes place at multiple levels of biological organisation, from local cell competition and immune crosstalk to organism‐wide metabolic and physiological collapse. Here, we integrate findings from Drosophila melanogaster studies that reveal conserved mechanisms through which tumours hijack host systems to ...
José Teles‐Reis, Tor Erik Rusten
wiley +1 more source
The mutational status of p53 can influence its recognition by human T-cells
p53 was reported to be an attractive immunotherapy target because it is mutated in approximately half of human cancers, resulting in its inactivation and often accumulation in tumor cells.
Katerina Shamalov +3 more
doaj +1 more source
Background While tumor suppressor p53 functions primarily as a transcription factor in the nucleus, cellular stress can cause p53 to translocate to the mitochondria and directly trigger a rapid apoptotic response. We have previously shown that fusing p53
Phong Lu +5 more
doaj +1 more source
Fos co-operation with PTEN loss elicits keratoacanthoma not carcinoma due to p53/p21WAF-induced differentiation triggered by GSK3b inactivation and reduced AKT activity [PDF]
To investigate gene synergism in multistage skin carcinogenesis, the RU486-inducible cre/lox system was employed to ablate PTEN function [K14.cre/D5PTENflx] in mouse epidermis expressing activated v-fos [HK1.fos].
Alexander, C.L. +5 more
core +1 more source

