No abstract

Background Belonging to the protein arginine methyltransferase (PRMT) family, the enzyme encoded by coactivator associated arginine methyltransferase 1 (CARM1) catalyzes the methylation of protein arginine residues, especially acts on histones and other chromatin related proteins, which is essential in regulating gene expression. Beyond its well-established involvement in the regulation of transcription, recent studies have revealed a novel role of CARM1 in tumorigenesis and development, but there is still a lack of systematic understanding of CARM1 in human cancers. An integrated analysis of CARM1 in pan-cancer may contribute to further explore its prognostic value and potential immunological function in tumor therapy. Results Based on systematic analysis of data in multiple databases, we firstly verified that CARM1 is highly expressed in most tumors compared with corresponding normal tissues, and is bound up with poor prognosis in some tumors. Subsequently, relevance between CARM1 expression level and tumor immune microenvironment is analyzed from the perspectives of tumor mutation burden, microsatellite instability, mismatch repair genes, methyltransferases genes, immune checkpoint genes and immune cells infiltration, indicating a potential relationship between CARM1 expression and tumor microenvironment. A gene enrichment analysis followed shortly, which implied that the role of CARM1 in tumor pathogenesis may be related to transcriptional imbalance and viral carcinogenesis. Conclusions Our first comprehensive bioinformatics analysis provides a broad molecular perspective on the role of CARM1 in various tumors, highlights its value in clinical prognosis and potential association with tumor immune microenvironment, which may furnish an immune based antitumor strategy to provide a reference for more accurate and personalized immunotherapy in the future.

Leukemia and lymphoma—the most common hematological malignant diseases—are often accompanied by complications such as drug resistance, refractory diseases and relapse. Amino acids (AAs) are important energy sources for malignant cells. Tumor‐mediated AA metabolism is associated with the immunosuppressive properties of the tumor microenvironment, thereby assisting malignant cells to evade immune surveillance. Targeting abnormal AA metabolism in the tumor microenvironment may be an effective therapeutic approach to address the therapeutic challenges of leukemia and lymphoma. Here, we review the effects of glutamine, arginine and tryptophan metabolism on tumorigenesis and immunomodulation, and define the differences between tumor cells and immune effector cells. We also comment on treatments targeting these AA metabolism pathways in lymphoma and leukemia and discuss how these treatments have profound adverse effects on tumor cells, but leave the immune cells unaffected or mildly affected.