Likun Cui's research while affiliated with Second Military Medical University, Shanghai and other places

Amino acid metabolism plays important roles in tumor biology and tumor therapy. Accumulating evidence has shown that amino acids contribute to tumorigenesis and tumor immunity by acting as nutrients, signaling molecules, and could also regulate gene transcription and epigenetic modification. Therefore, targeting amino acid metabolism will provide new ideas for tumor treatment and become an important therapeutic approach after surgery, radiotherapy, and chemotherapy. In this review, we systematically summarize the recent progress of amino acid metabolism in malignancy and their interaction with signal pathways as well as their effect on tumor microenvironment and epigenetic modification. Collectively, we also highlight the potential therapeutic application and future expectation.

Chemokines and their receptors play an important role in immune monitoring and immune defense during tumor growth and metastasis. However, their prognostic roles in pan-cancer have not been elucidated. In this work, we screened all chemokine receptors in pan-cancer and discovered X-C Motif Chemokine Receptor 1 (XCR1) as a reliable immunological and prognostic biomarker in pan-cancer using bioinformation. The TCGA database served as the foundation for the primary research database analysis in this work. XCR1 was downregulated in tumors. Patients with reduced XCR1 showed worse prognoses and a concomitant decrease in immune cell infiltration (DCs and CD8+ T cells). According to a gene enrichment study, XCR1 enhanced immune system performance by promoting T-cell infiltration through the C-X-C Motif Chemokine Ligand 9 (CXCL9)- C-X-C Motif Chemokine Receptor 3 (CXCR3) axis. In addition, XCR1 is mainly expressed in infiltrated DCs and some malignant cells in tumor tissues. Our data revealed the important role of XCR1 in remodeling the tumor microenvironment and predicting the survival prognosis, which could also be used as a sensitive biomarker for tumor immunotherapy.

Background Chemokines and their receptors play an important role in immune monitoring and immune defense during the tumor growth and metastasis. However, their prognostic roles in pan-cancer were not elucidated. In this work, we screened all chemokine receptors in pan-cancer and discovered XCR1 as a reliable immunological and prognostic biomarker in pan-cancer using bioinformation. Methods The TCGA database served as the foundation for the primary research database analysis in this work. The screening of tumor patients' overall survival yielded XCR1, which had a favorable predictive connection. Further investigation into the connection between XCR1 expression and tumor development stage in tumor patients was done using the clinicopathological stage. The regulatory mechanism of XCR1 regulating tumor formation and as a prognostic molecule has also been discovered using enrichment analysis of XCR1-related genes. The spatial localization of XCR1 in tumor tissues was discovered by using single-cell databases. Result XCR1 was downregulated in tumors. Patients with reduced XCR1 showed worse prognoses and a concomitant decrease in immune cell infiltration (DCs and CD8 + T cells). According to gene enrichment study, XCR1 enhanced immune system performance by promoting T cell infiltration through the CXCL9-CXCR3 axis. In addition, XCR1 is mainly expressed on infiltrated DCs and some malignant cells in tumor tissues. Conclusion Our data revealed the important role of XCR1 in remodeling of the tumor microenvironment and predicting the survival prognosis, which could also be used as sensitive biomarker for tumor immunotherapy.

MHC class I molecules are key in the presentation of antigen and initiation of adaptive CD8+ T cell responses. In addition to its classical activity, MHC I may possess nonclassical functions. We have previously identified a regulatory role of MHC I in TLR signaling and antibacterial immunity. However, its role in innate antiviral immunity remains unknown. In this study, we found a reduced viral load in MHC I-deficient macrophages that was independent of type I IFN production. Mechanically, MHC I mediated viral suppression by inhibiting the type I IFN signaling pathway, which depends on SHP2. Cross-linking MHC I at the membrane increased SHP2 activation and further suppressed STAT1 phosphorylation. Therefore, our data revealed an inhibitory role of MHC I in type I IFN response to viral infection and expanded our understanding of MHC I and antigen presentation.