Results 141 to 150 of about 1,802,261 (296)

AARS1‐Mediated H3K27 Lactylation Rewires Glycolysis to Sustain Aggressive and Recurrent Bladder Cancer

open access: yesAdvanced Science, EarlyView.
AARS1 drives PI3K–AKT–mTOR‐dependent glycolysis in bladder cancer, promoting lactate accumulation, increased lactylation, H3K27la enrichment at the HK2 promoter, and HK2 transcription. HK2 reinforces glycolysis, sustaining a metabolic–epigenetic program associated with tumor progression, recurrence, and metastasis.
Qin Yuan   +13 more
wiley   +1 more source

Epigenetic Reactivation of TNFRSF19 Suppresses Mitophagy and Sensitizes Triple‐Negative Breast Cancer to Doxorubicin

open access: yesAdvanced Science, EarlyView.
TNFRSF19 is an epigenetically silenced regulator of mitophagy in triple‐negative breast cancer. TNFRSF19 deficiency activates the TGFBR1–SMAD3–PINK1 axis to promote mitophagy and confer doxorubicin resistance, whereas decitabine‐mediated restoration of TNFRSF19 suppresses mitophagy and enhances doxorubicin sensitivity, revealing a targetable epigenetic–
Shiyang Liu   +7 more
wiley   +1 more source

Mutant KRAS‐m6A Epitranscriptome Axis Promotes Colorectal Cancer and is a Therapeutic Target

open access: yesAdvanced Science, EarlyView.
Mutant KRAS‐m6A axis promotes colorectal cancer (CRC) progression. Mutant KRAS stabilizes METTL3, leading to increased m6A‐modified BCL9L mRNA and translation of BCL9L protein. BCL9L in turn mediates TGF‐β secretion to induce differentiation of Treg and an immunosuppressive microenvironment.
Danyu Chen   +12 more
wiley   +1 more source

SOX30 Facilitates Triple‐Negative Breast Cancer Metastasis via TNFR2–NF‐κB Signaling and Tumor Microenvironment Remodeling

open access: yesAdvanced Science, EarlyView.
SOX30 drives triple‐negative breast cancer (TNBC) metastasis through a dual mechanism: direct activation of the TNFR2/NF‐κB signaling cascade and subsequent CCL20‐mediated recruitment of tumor‐associated macrophages (TAMs) into the tumor microenvironment.
Pingping Gao   +10 more
wiley   +1 more source

TP53 Loss Elevates NF‐κB‐IFN‐β‐MHC‐Ia Signaling to Promote NK Cell Resistance in Osteosarcoma

open access: yesAdvanced Science, EarlyView.
TP53 loss in a transforming or osteosarcoma cell promotes cytosolic DNA accumulation, activating NF‐κB‐dependent IFN‐β production. Autocrine IFN‐β signaling increases cell‐surface HLA‐Ia expression, strengthens inhibitory KIR signaling in natural killer cells, and thereby enables the affected cell to evade NK cell‐mediated cytotoxicity.
Guihui Qin   +9 more
wiley   +1 more source

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