Results 101 to 110 of about 383,521 (254)

Selenomethionine alleviates T-2 toxin-induced articular chondrocyte ferroptosis via the system Xc−/GSH/GPX4 axis

open access: yesEcotoxicology and Environmental Safety
T-2 toxin can induce bone and cartilage development disorder, and oxidative stress plays an important role in it. It is well known that selenomethionine (Se-Met) has antioxidative stress properties and promotes the repair of cartilage lesion, but it ...
Fang-fang Yu   +12 more
doaj   +1 more source

Colorectal cancer‐derived FGF19 is a metabolically active serum biomarker that exerts enteroendocrine effects on mouse liver

open access: yesMolecular Oncology, EarlyView.
Meta‐transcriptome analysis identified FGF19 as a peptide enteroendocrine hormone associated with colorectal cancer prognosis. In vivo xenograft models showed release of FGF19 into the blood at levels that correlated with tumor volumes. Tumoral‐FGF19 altered murine liver metabolism through FGFR4, thereby reducing bile acid synthesis and increasing ...
Jordan M. Beardsley   +5 more
wiley   +1 more source

Dimethyl fumarate combined with cisplatin at subcytotoxic doses sensitizes cervical cancer toward ferroptosis and apoptosis through GSH restriction and p53 (re)activation

open access: yesMolecular Oncology, EarlyView.
Dimethyl fumarate (DMF) reduces growth of HPV‐positive cervical cancer spheroids and induces ferroptosis in cervical cancer cells via blocking SLC7A11/Glutathione (GSH) axis. Combination of subcytotoxic doses of DMF and cisplatin (CDDP) further suppresses spheroid growth and drives cell death in 2D culture models.
Carolina Punziano   +6 more
wiley   +1 more source

Comparative Analysis of Gut Microbiota from Rats Induced by Se Deficiency and T-2 Toxin. [PDF]

open access: yesNutrients, 2023
Wu Y   +14 more
europepmc   +1 more source

Engineered extracellular vesicles enriched with the miR‐214/199a cluster enhance the efficacy of chemotherapy in ovarian cancer

open access: yesMolecular Oncology, EarlyView.
Loss of the miR‐214/199a cluster is associated with recurrence in ovarian cancer. Engineered small extracellular vesicles (m214‐sEVs) elevate miR‐214‐3p/miR‐199a‐5p in tumor cells, suppress β‐catenin, TLR4, and YKT6 signaling, reprogram tumor‐derived sEV cargo, reduce chemoresistance and migration, and enhance carboplatin efficacy and survival in ...
Weida Wang   +12 more
wiley   +1 more source

Establishment of a humanized patient‐derived xenograft mouse model of high‐grade serous ovarian cancer for preclinical evaluation of combination immunotherapy

open access: yesMolecular Oncology, EarlyView.
We have established a humanized orthotopic patient‐derived xenograft (Hu‐oPDX) mouse model of high‐grade serous ovarian cancer (HGSOC) that recapitulates human tumor–immune interactions. Using combined anti‐PD‐L1/anti‐CD73 immunotherapy, we demonstrate the model's improved biological relevance and enhanced translational value for preclinical ...
Luka Tandaric   +10 more
wiley   +1 more source

T-2 toxin induces senescence in human neuroblastoma SH-SY5Y cells by regulating the HIF-1α/p53/p21 pathway

open access: yesEcotoxicology and Environmental Safety
The mechanisms by which T-2 toxin induces senescence in neurons, along with the involvement of hypoxia-inducible factor-1α (HIF-1α), remain poorly understood. Using human neuroblastoma SH-SY5Y cells as a model, T-2 toxin (6 nM, 1–48 h) induced senescence
Yating Wang, Xu Wang, Qinghua Wu
doaj   +1 more source

Hippo pathway at the crossroads of stemness and therapeutic resistance in breast cancer

open access: yesMolecular Oncology, EarlyView.
Dysregulation of the Hippo pathway drives nuclear accumulation of YAP/TAZ, activating stemness‐related transcriptional programs that sustain breast cancer stemness and fuel therapeutic resistance across subtypes, underscoring Hippo signaling as a targetable vulnerability. Figure created and edited with BioRender.com.
Giulia Schiavoni   +11 more
wiley   +1 more source

Cell‐cycle‐specific lesion evolution rather than inhibition of double‐strand‐break repair underpins cisplatin radiosensitization

open access: yesMolecular Oncology, EarlyView.
We analyze cisplatin–DNA adducts (CDAs) and double‐strand breaks (DSBs) in a cell‐cycle‐dependent manner. We find that CDAs form similarly across all cell cycle phases. DSBs arise only in S‐phase. CDAs might not directly impair DSB repair, but S‐phase DSB lesions evolve in the presence of CDAs and disrupt repair in G2, also causing radiosensitization ...
Ye Qiu   +10 more
wiley   +1 more source

Home - About - Disclaimer - Privacy