RESUMO
Long non-coding RNAs (lncRNAs) are RNA sequences exceeding 200 nucleotides in length that lack protein-coding capacity and participate in diverse biological processes in the human body, particularly exerting a pivotal role in disease surveillance, diagnosis, and progression. Taurine upregulated gene 1 (TUG1) is a versatile lncRNA, and recent studies have revealed that the aberrant expression or function of TUG1 is intricately linked to the pathogenesis of liver diseases. Consequently, we have summarized the current understanding of the mechanism of TUG1 in liver diseases such as liver fibrosis, fatty liver, cirrhosis, liver injury, hepatitis, and liver cancer. Moreover, mounting evidence suggests that interventions targeting TUG1 or its downstream pathways may hold therapeutic promise for liver diseases. This review elucidates the characteristics, mechanisms, and targets of TUG1 in liver diseases, offering a theoretical basis for the prevention, diagnosis, treatment, and prognostic biomarkers of liver diseases.
Assuntos
Hepatopatias , RNA Longo não Codificante , Humanos , RNA Longo não Codificante/genética , Hepatopatias/genética , Hepatopatias/diagnóstico , Hepatopatias/metabolismoRESUMO
Cancer immunotherapy has shown promise in treating various malignancies. However, the presence of an immunosuppressive tumor microenvironment (TME) triggered by M2 tumor-associated macrophages (TAMs) and the limited tumor cell antigenicity have hindered its broader application. To address these challenges, we developed DOX/R837@ManL, a liposome loaded with imiquimod (R837) and doxorubicin (DOX), modified with mannose-polyethylene glycol (Man-PEG). DOX/R837@ManL employed a mannose receptor (MRC1)-mediated targeting strategy, allowing it to accumulate selectively at M2 Tumor associated macrophages (TAMs) and tumor sites. R837, an immune adjuvant, promoted the conversion of immunosuppressive M2 TAMs into immunostimulatory M1 TAMs, and reshaped the immunosuppressive TME. Simultaneously, DOX release induced immunogenic cell death (ICD) in tumor cells and enhanced tumor cell antigenicity by promoting dendritic cells (DCs) maturation. Through targeted delivery, the synergistic action of R837 and DOX activated innate immunity and coordinated adaptive immunity, enhancing immunotherapy efficacy. In vivo experiments have demonstrated that DOX/R837@ManL effectively eliminated primary tumors and lung metastases, while also preventing tumor recurrence post-surgery. These findings highlighted the potential of DOX/R837@ManL as a promising strategy for cancer immunotherapy.