Results 111 to 120 of about 148,781 (262)

REGγ Suppresses Ferroptosis and Induces Drug Resistance by Degrading WDR6 in Chondrosarcoma

open access: yesAdvanced Science, EarlyView.
Here, we identified REGγ as a susceptibility factor in chondrosarcoma. Our study demonstrates that abnormally activated REGγ‐20S proteasome promotes chondrosarcoma development and progression. Further validation in animal models revealed that blocking REGγ function induced ferroptosis, suppressed malignant progression of chondrosarcoma, and uncovered a
Fanrong Liu   +20 more
wiley   +1 more source

The E3 Ubiquitin Ligase RLIM Safeguards Oligodendrocyte Development and Myelination by Targeting SLC7A11 for Polyubiquitination to Regulate Ferroptotic Resistance

open access: yesAdvanced Science, EarlyView.
RLIM‐mediated SLC7A11 polyubiquitination is required for SPTBN2‐mediated trafficking and membrane localization of SLC7A11, which enables oligodendrocyte precursor cells to be resistant to ferroptosis and safeguards oligodendrocyte lineage progression and thus myelination.
Yuwei Li   +8 more
wiley   +1 more source

Self‐Sustaining Lactate Depletion Nanoplatform Remodels Tumor Microenvironment and Augments Synergistic Photodynamic/Photothermal/Chemodynamic/Starvation Therapy for Eradication of Colon Cancer

open access: yesAdvanced Science, EarlyView.
The HILA nanoplatform integrates HMnO2, LOX, and ICG to orchestrate multimodal therapy (starvation, chemodynamic, photodynamic, and photothermal) for achieving efficient colon cancer eradication. The established HMnO2‐LOX catalytic cycle continuously consumes lactate, acidifys microenvironment, relieves hypoxia, and generats reactive oxygen species ...
Yu‐E. Wang   +11 more
wiley   +1 more source

Targeting NSUN2‐Mediated m5C Modification Attenuates Chondrocyte Senescence and NLRP3 Activation in Osteoarthritis

open access: yesAdvanced Science, EarlyView.
NSUN2‐mediated m5C modification cooperates with ALYREF to stabilize and export IP3R3 mRNA, increasing IP3R3 expression and Ca2 + overload in chondrocytes. This signaling promotes mitochondrial dysfunction, NLRP3 inflammasome activation, and senescence, thereby accelerating osteoarthritis progression.
Guping Mao   +8 more
wiley   +1 more source

Modulation of Lung Adenocarcinoma by Phosphorylated FOXN3‐Mediated Transcriptional Inactivation of p53

open access: yesAdvanced Science, EarlyView.
In non‐tumorous lung tissues, FOXN3 promotes the transcriptional activation of p53 by facilitating its recruitment to target promoters, thereby suppressing lung tumorigenesis through activation of the p53 signaling pathway. Conversely, in lung adenocarcinoma tissues, hyperphosphorylated FOXN3 dissociates from the promoters of p53‐responsive genes and ...
Jinjin Yu   +16 more
wiley   +1 more source

TET1 Inhibition Promotes Therapeutic Sensitivity in TP53‐Mutant GBM by Influencing Genome Fragility and Altering TAMs Biology

open access: yesAdvanced Science, EarlyView.
In TP53mut GBM cells, reduced P53 function is associated with increased TET1 expression. Genetic or pharmacological inhibition of TET1 correlates with genome fragility, including DNA damage, cellular senescence, telomere shortening, and reactive oxygen species accumulation, which may contribute to increased efficacy of antitumor therapy.
Zhuonan Pu   +12 more
wiley   +1 more source

Histone H3K18 Lactylation Promotes the Malignant Progression of Wilms Tumor via a PSRC1/AKT/HIF‐1α Positive Feedback Loop

open access: yesAdvanced Science, EarlyView.
In nephroblastoma, aberrant glycolysis drives lactate accumulation, which elevates histone H3K18 lactylation via p300. Lactylation of the PSRC1 promoter activates its transcription. PSRC1 competitively binds AKT, relieving PTEN‐mediated inhibition and triggering AKT/mTOR/HIF‐1α signaling.
Yanping Wang   +6 more
wiley   +1 more source

Ubiquitination of ACSL4 by Parkin Suppresses Ferroptosis and Rescues Glucocorticoid‐Induced Bone Loss

open access: yesAdvanced Science, EarlyView.
GCs reduce Parkin, leading to ACSL4 accumulation and PUFA‐phospholipid‐driven ferroptosis in BMSCs, which impairs osteogenesis and promotes adipogenesis, causing GIOP. Parkin restoration (via OE‐Parkin or Parkin‐LNP@DSS6) ubiquitinates and degrades ACSL4, inhibiting ferroptosis, rescuing bone formation, and rescues GIOP bone loss.
Li‐jiang Han   +16 more
wiley   +1 more source

Home - About - Disclaimer - Privacy