CAV2 (Caveolin 2)

Our study establishes a novel multi-gene diagnostic signature for oxaliplatin resistance through integrative bioinformatics and machine learning approaches. The comprehensive molecular characterization and identification of potential therapeutic candidates provide new insights into resistance mechanisms and clinical management strategies for oxaliplatin-resistant colorectal cancer.

This interplay observed between cancer cells, neurons, and glial cells suggests a potential mechanism through which tumor-associated nerves might influence cancer stemness via metabolic reprogramming. This highlights a possible direction for anticancer therapy that warrants further investigation.

LPHN1 stimulation by LTXN4C induced a small Ca2+ release sensitive to thapsigargin, and a strong, gradual influx of Ca2+, which was insensitive to thapsigargin...These channels mediate an initial Ca2+ influx that triggers Ca2+-induced Ca2+ release and SOCE. This mechanism, elucidated in model cells, can explain how LTXN4C stimulates neurotransmitter release.

Our previous studies demonstrated that ciprofloxacin inhibits erastin-induced ferroptosis by enhancing glutathione peroxidase 4 (GPX4) protein stability. These findings reveal a dual role of ciprofloxacin in ferroptosis regulation, dependent on the specific stimuli and downstream signaling pathways activated. This dual functionality highlights the potential therapeutic implications of ciprofloxacin in modulating ferroptosis in disease contexts.

These findings demonstrate that surface biotinylation improves the sensitivity and selectivity of plasma membrane proteomics under hypoxia, revealing hypoxia-responsive proteins and pathways not captured by standard whole-cell analysis.

Our findings demonstrate that CAV1 exerts its anti-tumor effects, at least in part, by inhibiting EGFR degradation and modulating the AKT/STAT3 pathway, as well as enhancing the Bax/Caspase-3/Bcl-2 signaling pathway in LUAD cells. These results suggest that targeting CAV1 may represent a promising therapeutic strategy for the treatment of LUAD patients.

Alteration of CAV2 disrupted lipid homeostasis and inhibited OSCC progression by affecting key processes, including apoptosis, lipolysis, and mitochondrial dysfunction. The disruption was driven by the dysregulation of the PPARγ/NCOR1 axis, highlighting the potential of targeting CAV2 and its interaction with PPARγ as a therapeutic strategy for OSCC.

Our findings provide new insights into the molecular basis of NB, identifying four novel biomarkers and developing a risk scoring model based on four co-expressed genes. This model has the potential to become an effective tool for predicting prognosis and guiding treatment in NB patients.

The role of M2 macrophages in tumor progression could anticipate the prognosis of LUAD and develop novel immunotherapy strategies.

FOLFIRI, a combination of folinic acid, 5-Fluorouracil, and Irinotecan, is one of the recommended first-line chemotherapeutic treatments for metastatic colorectal cancer (mCRC). Our analyses revealed a five-gene FOLFIRI resistance signature associated with RFS that may help to predict FOLFIRI resistance and thus avoid unnecessary ineffective treatment. Signature members might also represent targets to fight FOLFIRI resistance.

This study provides evidence for the ability of OT to regulate caveolin and PTRF expression. This study elucidates possible mechanisms by which cell receptors and caveolae proteins interact to enhance cell proliferation.

Our results suggest that the LD-M risk score is an effective prognostic indicator for individualized treatment of LUAD.