AI Networking Cookbook: Practical recipes for AI-assisted network automation and development
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It is found that KAT2B transcriptionally activates GSTZ1 in a H3K9ac-dependent manner, which in turn inhibits GPX4 expression, thereby suppressing OSCC proliferation and stemness while enhancing ferroptosis sensitivity.
ABSTRACT Background Oral squamous cell carcinoma (OSCC) is a prevalent malignancy associated with poor outcomes, largely attributable to cisplatin resistance—the standard chemotherapeutic agent. Aims While ferroptosis has been proposed as a promising therapeutic target, how it is regulated in OSCC remains largely uncle...
ABSTRACT Glioblastoma multiforme (GBM), the most lethal type of primary brain tumor, exhibits profound metabolic plasticity driven by glioma stem cells (GSCs), which sustain therapeutic resistance and tumor recurrence. Here, we elucidate a novel epigenetic‐metabolic axis mediated by the histone acetyltransferase KAT7 t...
A KLF5-G6PD-SLC7A11 axis is identified as a critical metabolic safeguard against ferroptosis in LUSC, and targeting G6PD disrupts mitochondrial homeostasis, enhances mitophagy-dependent oxidative stress, and sensitizes tumors to ferroptotic therapy, highlighting a promising therapeutic strategy for LUSC.
A novel METTL3/ELF1/GPX4 axis through which METTL3 promotes TNBC growth by regulating oxidative stress and ferroptosis-related markers is suggested, providing a basis for further investigation of this pathway in the context of TNBC biology and therapeutic development.
An METTL3-STK25-YAP-GPX4 regulatory model that links epitranscriptomic control to ferroptosis susceptibility and tumor growth in OS is supported and warrants further preclinical and prospective clinical validation.
It is suggested that NFS1 functions as an oncogenic driver, as well as a promising prognostic biomarker and therapeutic target in osteosarcoma, and linking metabolic reprogramming to ferroptosis resistance, is suggested.
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