OLR1 (Oxidized Low Density Lipoprotein Receptor 1)

BaA promotes LUAD progression via multi-target regulation and tumor immune microenvironment remodeling. This study offers an integrated computational framework and an AOP-based theoretical foundation for assessing pollutant health risks and informing targeted LUAD interventions.

Our established nomogram effectively predicted the 1-, 3-, and 5-year OS probabilities in patients with GC (C-index [95% CI] = 0.649 [0.624-0.675]). OLR1 is strongly associated with a dismal prognostic outcome and immune cell infiltration in patients with GC.

Furthermore, treatment with the antioxidant resveratrol (RSV) and its nanoformulation (RSV-NPs) markedly inhibited tumor growth in mice with lipid metabolic disorders, highlighting their potential to counteract progesterone resistance by disrupting this OLR1/FOXM1/FGF19 axis. This work highlights the therapeutic potential of targeting the tumor-stroma metabolic axis to increase progesterone sensitivity and improve outcomes in EC patients with fertility-preserving demands.

In conclusion, CRP facilitates progression of LOX-1-expressing cervical cancer by stimulating LOX-1 and its downstream effectors in cancer cells and MDSCs. Novel treatments targeting CRP or LOX-1 may be against LOX1-expressing cancer.

Moreover, drug sensitivity analysis and molecular docking studies have indicated that simvastatin and pazopanib are potential inhibitors of OLR1. These findings suggest that simvastatin and pazopanib could open up innovative potential therapeutic avenues for individuals with HNSCC.

IGF2BP2 recognizes and stabilizes LOX1 through m6A modification, contributing to TAN-mediated LUAD progression. Overall, these findings offer new insights into LUAD progression and demonstrate that IGF2BP2 is a key regulator that promotes tumor advancement, highlighting the IGF2BP2-LOX1 axis as a potential therapeutic target for LUAD.

In summary, this study proposes a new prognostic signature for patients with LUAD based on M2 TAM and angiogenesis-related genes. The signature forecasts the prognosis of LUAD by an independent manner, reveals the potential molecular mechanisms involved in tumor immune-related functions, and offers appropriate clinical strategies for the treatment of patients with LUAD.

PRRX1 promotes OLR1 expression by recruiting H3K27ac and H3K4me3, activating CAFs, and thereby promoting the growth, migration, and immune evasion of lung cancer cells.

Our study uncovers the significance of the let-7d-5p-OLR1 axis in OSCC pathogenesis, offering novel insights for future therapeutic interventions.

Although there was no significant correlation between the gene expression pattern observed in dysplastic keratinocytes and the primary tumor of the HNSCC group, we could identify an exotic gene that was seldom discussed in association with cancer, viz., OLR1. Exploration into other top-ranking differentially expressed genes in dysplastic cases would aid in identifying the candidate gene associated with both phenotypes.

Moreover, OLR1 expression may affect EMT, stemness, and cuproptosis resistance outcomes. OLR1 is an immune-related prognostic biomarker with potential as a prognostic indicator for immunotherapy, and it may also be involved in regulating the EMT process and cuproptosis in HNSCC.