LAPTM5 (Lysosomal Protein Transmembrane 5)

Preclinical data link LAPTM5 to stroke outcomes via stress-kinase and lysosomal pathways, while LAPTM4A and LAPTM4B associate with glioma progression, immune evasion, and therapy resistance. Overall, LAPTM proteins represent promising biomarkers and therapeutic targets, warranting cell-type-resolved validation and central nervous system (CNS)-optimized delivery strategies, including gene therapy, small-molecule/degrader approaches, and multi-omics-guided patient stratification.

These findings identify LAPTM5 as a key regulator of TGF-β/Smad-driven epithelial plasticity and omental dissemination in HGSOC, positioning it as both a prognostic biomarker and a potential therapeutic target for advanced-stage disease.

Our cross-disease analysis unveils a conserved GMP-TAM myeloid remodeling axis in glioma. The derived RS model may serve as a powerful marker for predicting prognosis, and also for predicting the benefits derived from immunotherapy, offering a novel tool for precision immunotherapy in glioma.

Additionally, 12 drugs sensitive to EC were identified. This study establishes a prognostic model based on efferocytosis-associated genes for EC, providing clinical guidance for the prognosis and treatment of EC patients.

Our findings reveal that LINC02888 drives HGSOC progression through a mechanism involving PPIB-mediated stabilization of LAPTM5 mRNA, which suppresses RIG-I-like receptor signaling. It also appropriately suggests that inhibiting this innate immune pathway may contribute to an immunosuppressive tumor microenvironment, making the LINC02888-PPIB-LAPTM5 axis a promising therapeutic target for this aggressive malignancy.

LAPTM5 knockdown increases lysosomal membrane permeability, leading to the release of cathepsin D (CTSD), which elevates intracellular reactive oxygen species (ROS) levels; further destabilizing the lysosomal membrane and accelerating cell death. Our findings elucidate the mechanism by which LAPTM5 contributes to cisplatin resistance through lysosomal membrane stabilization and identify LAPTM5 as a potential therapeutic target for overcoming cisplatin resistance in NSCLC.

This work identifies new genes that influence ageing and AD pathogenesis, and highlights the importance of microglia and oligodendrocytes in the resilience of the brain against ageing and AD pathogenesis. Our findings have implications for developing markers indicating the physiological age of the brain and new targets for therapeutic intervention.

GALNT6 is integral to the resistance mechanisms against lenvatinib in HCC by modulating autophagy and CAF activation. Targeting GALNT6 offers a promising strategy to enhance lenvatinib efficacy and improve therapeutic outcomes in HCC.

In this context, further preclinical research is essential to validate LAPTM5 as a potential target for diagnosis, therapy, and prognosis in immune-related disorders and tumors. This review summarized the current insights into LAPTM5's role in tumors and immune-related deficits, highlighting its potential as a valuable biomarker and therapeutic target.

Finally, drug prediction yielded three potential drugs: Lenvatinib, methadone, and trimethoprim. PCD-related biomarkers in LUAD were explored, which may contribute to further understanding on PCD in LUAD.

The key gene ARHGAP25 identified through bioinformatics for lung cancer bone metastasis was significantly downregulated. Its low expression constitutes an independent risk factor for secondary bone metastatic disease in patients with lung carcinoma.

This article summarizes the characteristics of the LAPTM5 gene and protein structure and provides a comprehensive review of the mechanisms involved in cell death, autophagy, immunity, and inflammation regulation. It emphasizes the significance of LAPTM5 in the clinical prevention and treatment of cardiovascular diseases, immune system disorders, viral infections, cancer, and other diseases, which could provide new therapeutic ideas and targets for human diseases.