PRMT1 reverts the immune escape of necroptotic colon cancer through RIP3 methylation

He, Yongmei; Jiang, Yi; Wu, Qi; Liu, Yanchen; Xie, Qingqiang; Zou, Yuxiu; Wu, Jiaqian; Zhang, Chundong; Zhou, Zhongjun; Bian, Xiu‐Wu; Jin, Guoxiang

doi:10.1038/s41419-023-05752-w

Cited by 6 publications

(3 citation statements)

References 39 publications

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“…PRMT1 participates in the asymmetric dimethylation modification of arginine 3 on histone H4, necrotic apoptosis, and immune regulation in CRC [ 35 – 37 ]. Here, we identified a novel function of PRMT1 in abnormal glycolysis in CRC.…”

Section: Discussionmentioning

confidence: 99%

PRMT1-mediated PGK1 arginine methylation promotes colorectal cancer glycolysis and tumorigenesis

Liu,

Chen,

Wang

et al. 2024

Cell Death Dis

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Many types of cancer cells, including colorectal cancer cells (CRC), can simultaneously enhance glycolysis and repress the mitochondrial tricarboxylic acid (TCA) cycle, which is called the Warburg effect. However, the detailed mechanisms of abnormal activation of the glycolysis pathway in colorectal cancer are largely unknown. In this study, we reveal that the protein arginine methyltransferase 1 (PRMT1) promotes glycolysis, proliferation, and tumorigenesis in CRC cells. Mechanistically, PRMT1-mediated arginine asymmetric dimethylation modification of phosphoglycerate kinase 1 (PGK1, the first ATP-producing enzyme in glycolysis) at R206 (meR206-PGK1) enhances the phosphorylation level of PGK1 at S203 (pS203-PGK1), which inhibits mitochondrial function and promotes glycolysis. We found that PRMT1 and meR206-PGK1 expression were positively correlated with pS203-PGK1 expression in tissues from colorectal cancer patients. Furthermore, we also confirmed that meR206-PGK1 expression is positively correlated with the poor survival of patients with colorectal cancer. Our findings show that PRMT1 and meR206-PGK1 may become promising predictive biomarkers for the prognosis of patients with CRC and that arginine methyltransferase inhibitors have great potential in colorectal cancer treatment.

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Section: Discussionmentioning

confidence: 99%

PRMT1-mediated PGK1 arginine methylation promotes colorectal cancer glycolysis and tumorigenesis

Liu,

Chen,

Wang

et al. 2024

Cell Death Dis

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“…Mechanistically, PRMT1 methyltransferase is reportedly accountable for the methylation of RIP3, a central factor that accelerates necroptosis. This process of methylation obstructs the initiation of necroptosis by hindering the phosphorylation of RIP3, ultimately preventing the progression of tumor immune escape and necrotic colon cancer due to the initiation of necroptosis [ 119 ]. It has been found that PRMT1 could alleviate anemia symptoms in MDS patients [ 120 ].…”

Section: Prostate Cancermentioning

confidence: 99%

PRMT1 in human neoplasm: cancer biology and potential therapeutic target

Shen,

Zhou,

Xiao

et al. 2024

Cell Commun Signal

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Protein arginine methyltransferase 1 (PRMT1), the predominant type I protein arginine methyltransferase, plays a crucial role in normal biological functions by catalyzing the methylation of arginine side chains, specifically monomethylarginine (MMA) and asymmetric dimethylarginine (ADMA), within proteins. Recent investigations have unveiled an association between dysregulated PRMT1 expression and the initiation and progression of tumors, significantly impacting patient prognosis, attributed to PRMT1’s involvement in regulating various facets of tumor cell biology, including DNA damage repair, transcriptional and translational regulation, as well as signal transduction. In this review, we present an overview of recent advancements in PRMT1 research across different tumor types, with a specific focus on its contributions to tumor cell proliferation, metastasis, invasion, and drug resistance. Additionally, we expound on the dynamic functions of PRMT1 during distinct stages of cancer progression, elucidating its unique regulatory mechanisms within the same signaling pathway and distinguishing between its promotive and inhibitory effects. Importantly, we sought to provide a comprehensive summary and analysis of recent research progress on PRMT1 in tumors, contributing to a deeper understanding of its role in tumorigenesis, development, and potential treatment strategies.

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“…Additionally, RIPK3 can be activated following a domain-dependent interaction of the RIP-homotypic interaction motif (RHIM) due to the activation of TLR3 by double-stranded RNA (dsRNA) within endosomes and TLR4 activation by lipopolysaccharide (LPS) or DAMPs at the plasma membrane. RIPK3 catalyzes the phosphorylation of MLKL, leading to the formation of MLKL oligomers (trimers or tetramers) and their translocation to the plasma membrane, where they bind to specific phosphatidylinositol phosphate species [ 129 , 130 ].…”

Section: Cell Death Mechanisms Activated By Mtb Virulence Factors: Th...mentioning

confidence: 99%

Virulence Factors of Mycobacterium tuberculosis as Modulators of Cell Death Mechanisms

et al. 2023

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Mycobacterium tuberculosis (Mtb) modulates diverse cell death pathways to escape the host immune responses and favor its dissemination, a complex process of interest in pathogenesis-related studies. The main virulence factors of Mtb that alter cell death pathways are classified according to their origin as either non-protein (for instance, lipomannan) or protein (such as the PE family and ESX secretion system). The 38 kDa lipoprotein, ESAT-6 (early antigen-secreted protein 6 kDa), and another secreted protein, tuberculosis necrotizing toxin (TNT), induces necroptosis, thereby allowing mycobacteria to survive inside the cell. The inhibition of pyroptosis by blocking inflammasome activation by Zmp1 and PknF is another pathway that aids the intracellular replication of Mtb. Autophagy inhibition is another mechanism that allows Mtb to escape the immune response. The enhanced intracellular survival (Eis) protein, other proteins, such as ESX-1, SecA2, SapM, PE6, and certain microRNAs, also facilitate Mtb host immune escape process. In summary, Mtb affects the microenvironment of cell death to avoid an effective immune response and facilitate its spread. A thorough study of these pathways would help identify therapeutic targets to prevent the survival of mycobacteria in the host.

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PRMT1 reverts the immune escape of necroptotic colon cancer through RIP3 methylation

Cited by 6 publications

References 39 publications

PRMT1-mediated PGK1 arginine methylation promotes colorectal cancer glycolysis and tumorigenesis

PRMT1-mediated PGK1 arginine methylation promotes colorectal cancer glycolysis and tumorigenesis

PRMT1 in human neoplasm: cancer biology and potential therapeutic target

Virulence Factors of Mycobacterium tuberculosis as Modulators of Cell Death Mechanisms

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