Results 81 to 90 of about 2,151,650 (259)
Journal of Cancer Research and Practice, 2014 Background: Overexpression of DNA 5’-cytosine-methyltransferases (DNMTs), which silence genes including tumor suppressor genes, is involved in many cancers. However, the mechanism of DNMT overexpression remains mostly unclear.
Yen-An Tang +5 more
doaj +1 more source
The VHL tumor suppressor at the crossroad of protein folding, aggregation, and cancer
Molecular Oncology, EarlyView.Mutations, environmental stress, and chaperone dysfunction can destabilize pVHL, promoting its conversion from the native folded state into amyloid‐like assemblies. This transition may contribute to protein storage, cell dormancy, survival, and drug resistance.
Lara Abad +2 more
wiley +1 more source
Global re‐wiring of p53 transcription regulation by the hepatitis B virus X protein
Molecular Oncology, 2016 Background The tumour suppressor p53 is a central player in transcription regulation and cell fate determination. By interacting with p53 and altering its sequence‐specific binding to the response elements, the hepatitis B virus X protein (HBx) was ...
Cheryl Chan +6 more
doaj +1 more source
Molecular Oncology, EarlyView.In head and neck squamous cell carcinoma (HNSCC) p53 and p63 exert opposite roles on the transcription regulation of the lncRNA NEAT1. Under basal conditions, p53 levels are low and p63 represses NEAT1 expression. Upon genotoxic stress, p53 is rapidly induced, displacing p63 from the NEAT1 promoter leading to NEAT1 transcriptional activation and ...
Sara De Domenico +5 more
wiley +1 more source
Molecular Oncology, EarlyView.The kinase SRPK1 directly interacts with the protein TOPBP1 and regulates the pre‐mRNA splicing of WIZ thereby contributing to the activation of the ATR/CHK1 replicative checkpoint in response to replicative stress. This allows cancer cells' genomic stability and survival.
Amani Shreim +17 more
wiley +1 more source
Association of Interactions between Metabolic 'Caretaker' Genes, p53, MDM2, and Tobacco Use with the Risk of Oral Cancer: A Multifactor Dimensionality Reduction Approach. [PDF]
Asian Pac J Cancer Prev, 2023 Singh RD, Patel KA, Patel JB, Patel PS.
europepmc +1 more source
Mutant p53R273H disrupts PDPK1 homodimerization and contributes to PDPK1 activation
Molecular Oncology, EarlyView.How mutant p53R273H drives AKT signaling is unclear. We show that p53R273H, but not wild‐type, directly binds PDPK1 via a mutation‐dependent conformational change. This interaction disrupts inhibitory PDPK1 homodimerization and enhances AKT phosphorylation.
Mei Chee Lim +11 more
wiley +1 more source
Mutant p53 stimulates cell invasion through an interaction with Rad21 in human ovarian cancer cells
Scientific Reports, 2017 Missense mutations of TP53 are extremely common, and mutant p53 accumulation and gain-of-function play crucial roles in human ovarian cancer. Here, we investigated the role of mutant p53 in cell migration and invasion as well as its underlying molecular ...
Ji-Hye Ahn +3 more
doaj +1 more source
p53 induces distinct epigenetic states at its direct target promoters
BMC Genomics, 2008 Background The tumor suppressor protein p53 is a transcription factor that is mutated in many cancers. Regulation of gene expression by binding of wild-type p53 to its target sites is accompanied by changes in epigenetic marks like histone acetylation ...
Junk Damian J +3 more
doaj +1 more source
Targeting the EpCAM‐AXL axis to overcome drug resistance in lung cancer
Molecular Oncology, EarlyView.Lung cancer cells often evade therapy by hijacking signaling pathways. We reveal that cleaved EpCAM (sEpCAM) stabilizes the oncogenic protein AXL, driving NF‐κB and STAT3‐mediated chemoresistance. This EpCAM‐AXL axis identifies a high‐risk patient subset with poor prognosis.
Alexa Guerrero‐Alba +5 more
wiley +1 more source