SLC7A5 (Solute Carrier Family 7 Member 5)

In agreement, molecular docking analyses identified sterol-binding pockets. The data on both cholesterol and oxysterols suggests that ASC1 regulation may rely on a structurally specific sterol-protein interaction rather than general alterations of membrane biophysics, with potential relevance for conditions characterized by altered membrane cholesterol composition in cholesterol-rich tissues.

Our findings highlight the role of amino acid transporters in GAE. The proteome analysis reveals distinct patterns in GB with epilepsy and also underscores the influence of xCT expression on the tumor proteome, which could inform the development of targeted anti-seizure medication.

Clinical analysis further establishes that elevated PSMD14 and BCKDK expression in GBM correlates with decreased CD8+ T and NK cell infiltration and poorer patient survival. These findings highlight the PSMD14-BCKDK axis as a central regulator of tumor metabolic adaptation and immune suppression, and support PSMD14 inhibition-alone or in combination with CAR-NK therapy-as a promising strategy for precision immunometabolic intervention in GBM.

In vivo experiments showed that SLC7A5 overexpression accelerated the growth of mouse xenograft tumors. Consistent with the in vitro functional assays, Ki-67 and phosphorylated mTOR levels were also elevated in tumor tissues, further validating the association between SLC7A5 and mTOR-mediated tumor progression.

Importantly, CPCs-JPH promotes dendritic cell maturation, activates CD8+ T-cell responses, and significantly improves survival outcomes in orthotopic 4 T1 tumor-bearing mice. This work establishes a multifunctional and enzyme-responsive nanoplatform that harnesses ferroptosis to overcome therapeutic resistance while concurrently engaging innate and adaptive immunity in TNBC.

In vivo, rAGR2 accelerated tumor growth in melanoma and lung cancer models, accompanied by increased TAM accumulation, a shift toward M2 polarization, and suppressed T-cell function. AGR2 drives tumor progression by reprogramming TAMs toward an M2 phenotype and attenuating T-cell function via the CD98hc-xCT/p-ERK pathway, highlighting its potential as both a prognostic marker and a therapeutic target.

Plasma cell-specific deletion of Myd88 led to reduced survival and antibody secretion by antigen-specific cells in vivo and unresponsiveness to BAFF and APRIL ex vivo. These data reveal novel regulators that link plasma cell secretory capacity and lifespan.

Genetic variants in ASCT2 and LAT1-related genes are independently associated with survival in CRC, supporting the growing body of evidence supporting personalized medicine and highlighting the need to consider both genetic and tumor heterogeneity when defining risk and tailoring treatment strategies.

Bone metastasis is an adverse prognostic factor for progression-free survival in lung adenocarcinoma patients treated with third-generation EGFR-TKIs. Bone metastasis lesions exhibit a distinct immunosuppressive tumor microenvironment in EGFR-mutant advanced lung adenocarcinoma, in which upregulation of immune regulatory genes in cancer cells and dysfunction of immune cells may constitute a potential mechanism underlying resistance to third-generation EGFR-TKIs.

Inhibiting this signaling axis in combination with radiotherapy impairs intracranial xenograft growth, resulting in significant survival extensions for treated animals. Overall, our findings uncover a previously unrecognized regulatory axis where PRMT5-mediated R124me2s governs YAP activation through a feedback mechanism, presenting novel therapeutic vulnerabilities in GBM.

Tumor uptake of Cys-PEG5-IR was significantly higher than the unlabeled IR in the subcutaneous MDA-MB-231 TNBC xenograft. This work highlights the prospect of using methionine (Met) transport pathway as an alternative strategy for targeting cancer cells, especially TNBC cells.

Notably, glutamate depletion enhances the efficacy of neoadjuvant immunochemotherapy. Our findings provide insights into how the METTL3/m6A/CD98 axis-mediated regulation of glutamate efflux may sensitize HNSCC to neoadjuvant immunochemotherapy.