Results 171 to 180 of about 1,472,454 (309)

Mechanisms and therapeutic opportunities of the ribotoxic stress response in cancer

open access: yesMolecular Oncology, EarlyView.
Cancer cells' high translational demand creates opportunities to therapeutically target ribosome function. Ribosome stalling and collisions activate ZAKα and the ribotoxic stress response (RSR), which can trigger rapid, p53‐independent apoptosis in cancer.
Anastassiya Kim   +7 more
wiley   +1 more source

The VHL tumor suppressor at the crossroad of protein folding, aggregation, and cancer

open access: yesMolecular 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

A role for eIF5A in translational control of stress‐inducible proteins in multiple myeloma cell lines

open access: yesMolecular Oncology, EarlyView.
Loss of eIF5A rewires thapsigargin‐mediated endoplasmic reticulum stress responses in multiple myeloma cells by selective translation of mRNA transcripts, consequently dampening thapsigargin‐induced unfolded protein response (UPR) activation and shifting the balance from induction of apoptosis toward cell survival and proliferation.
Demi Both   +7 more
wiley   +1 more source

RNA Interference [PDF]

open access: yesBioMed Research International, 2006
Sioud, Mouldy, Haoudi, Abdelali
openaire   +2 more sources

Regulation of the lncRNA NEAT1 by p53‐ΔNp63 crosstalk modulates the DNA damage response and therapeutic efficacy in HNSCC

open access: yesMolecular 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

p190A/ARHGAP35 and p190B/ARHGAP5 proteins in endometrial cancer: a novel cancer‐relevant paralog interplay

open access: yesMolecular Oncology, EarlyView.
This study identifies ARHGAP5, in addition to the frequently mutated ARHGAP35, as significantly mutated in endometrial cancer. Mutations in both genes co‐occur and are associated with their correlated downregulation. Functional CRISPR studies show that both paralogs regulate similar pathways, including actin cytoskeleton organization.
Mathilde Pinault   +12 more
wiley   +1 more source

Extracellular matrix remodeling and immune reprogramming drive residual tumor progression of liver cancer after incomplete microwave ablation

open access: yesMolecular Oncology, EarlyView.
Incomplete microwave ablation (iMWA) of liver cancer triggers a biphasic progression in residual tumors. At Day 3, the microenvironment is characterized by acute inflammatory responses and extracellular matrix (ECM) remodeling. By Day 14, a profound shift occurs toward oncogenic signal transduction and immunosuppression, marked by macrophage ...
Yu Liu   +9 more
wiley   +1 more source

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