Emerging roles of non-coding RNAs in the metabolic reprogramming of tumor-associated macrophages

Li, Jiali; Lu, Zhenyi; Zhang, Ying; Xia, Lin; Su, Zhaoliang

doi:10.1016/j.imlet.2021.02.003

Cited by 8 publications

(5 citation statements)

References 105 publications

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“…Extracellular vesicles (including miR-30c and miR-let-7a, among several others) are secreted into TAMs through hypoxia-induced cancer cells, suppressing the glycolysis-related metabolic pathway AKT/mTOR in TAMs. Decreased glucose metabolism then raises M2-type associated factors including TGF-β, COX-2, IL-6, and ARG-1, reduces M1-type related factors including TNF-α, IL-12, and IL-1β, resulting in M2-type macrophage rewiring and tumor growth and angiogenesis ( 215 ). TAM, Tumor-associated macrophages: HIF-1α, Hypoxia-inducible factor 1-alpha; mTOR, mammalian target of rapamycin; ARG-1, Arginase 1; IL, Interleukin; COX-2, cyclooxygenase 2; TGF-β, Transforming growth factor beta; TNF-α, Tumor necrosis factor alpha.…”

Section: Mirnas and Metabolic Regulation In Immune Cells During Cancermentioning

confidence: 99%

Metabolic reprogramming by miRNAs in the tumor microenvironment: Focused on immunometabolism

et al. 2022

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MicroRNAs (miRNAs) are emerging as a significant modulator of immunity, and their abnormal expression/activity has been linked to numerous human disorders, such as cancer. It is now known that miRNAs potentially modulate the production of several metabolic processes in tumor-associated immune cells and indirectly via different metabolic enzymes that affect tumor-associated signaling cascades. For instance, Let-7 has been identified as a crucial modulator for the long-lasting survival of CD8+ T cells (naive phenotypes) in cancer by altering their metabolism. Furthermore, in T cells, it has been found that enhancer of zeste homolog 2 (EZH2) expression is controlled via glycolytic metabolism through miRNAs in patients with ovarian cancer. On the other hand, immunometabolism has shown us that cellular metabolic reactions and processes not only generate ATP and biosynthetic intermediates but also modulate the immune system and inflammatory processes. Based on recent studies, new and encouraging approaches to cancer involving the modification of miRNAs in immune cell metabolism are currently being investigated, providing insight into promising targets for therapeutic strategies based on the pivotal role of immunometabolism in cancer. Throughout this overview, we explore and describe the significance of miRNAs in cancer and immune cell metabolism.

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Section: Mirnas and Metabolic Regulation In Immune Cells During Cancermentioning

confidence: 99%

Metabolic reprogramming by miRNAs in the tumor microenvironment: Focused on immunometabolism

et al. 2022

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“…Cancer cells and TAMs establish a mutual metabolic communication, with cancer cells promoting the M2-like phenotype through the secretion of lactate, and TAMs increasing glucose availability for tumor cells [84]. Non-coding RNAs are crucial mediators of this interplay [85,86].…”

Section: Non-coding Rnas In the Regulation Of Bc Cells And Tam Metabo...mentioning

confidence: 99%

Non-Coding RNAs in the Crosstalk between Breast Cancer Cells and Tumor-Associated Macrophages

Benedetti

Turco

Fontemaggi

et al. 2022

ncRNA

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Non-coding RNAs (ncRNAs) play a pivotal role in regulating the tumor microenvironment (TME) by controlling gene expression at multiple levels. In tumors, ncRNAs can mediate the crosstalk between cancer cells and other cells in the TME, such as immune cells, stromal cells, and endothelial cells, influencing tumor development and progression. Tumor-associated macrophages (TAMs) are among the most abundant inflammatory cells infiltrating solid cancers that promote tumorigenesis, and their infiltration correlates with a poor prognosis in many tumors. Cancer cells produce different ncRNAs that orchestrate TAM recruitment and polarization toward a tumor-promoting phenotype. Tumor-reprogrammed macrophages shape the TME by promoting angiogenesis and tissue remodeling, and suppressing the anti-tumor activity of adaptive immune cells. TAMs can also produce ncRNA molecules that boost cancer cell proliferation and direct their phenotype and metabolic changes facilitating cancer progression and metastasis. This review will focus on the crosstalk between cancer cells and TAMs mediated by microRNAs and long non-coding RNAs during breast cancer (BC) initiation and progression.

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“…Therefore, controlling macrophages metabolic reprogramming may be new therapeutic approaches for cancer. Dong et al has reported that long noncoding RNAs (lncRNAs) engaged in the M2 polarization and metabolic of both cancer cells and macrophages [12,13]. The lncRNA colorectal neoplasia differentially expressed (lncRNA CRNDE), a 1910-nt lncRNA, has been found to be involved in osteoarthritis [15], delayed encephalopathy [16], and tumor progress [17,18].…”

Section: Introductionmentioning

confidence: 99%

LncRNA CRNDE promotes hepatoma cell proliferation by regulating the metabolic reprogramming of M2 macrophages via ERK pathway

Lin,

Jiang,

et al. 2024

Cancer Cell Int

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Background LncRNA colorectal neoplasia differentially expressed (CRNDE) was found to be an important regulator in many cancers. This project focuses on the function of CRNDE on macrophage metabolic reprogramming and Hepatocellular carcinoma (HCC). Method qRT-PCR and Immunofluorescence were used to analyze Arg-1, IL-10, CD163, CCL-18, CD206, and CRNDE expression in HCC tissues and macrophages. Western Blotting was used to analyze ERK and p-ERK expression. Edu assay, transwell assay and xenograft experiments were carried out to study cell viability, migrated and invasive capability. Immunohistochemical staining was used to evaluate Ki67 expression. A liquid chromatography-tandem mass spectrometry (LC-MS/MS) was performed for macrophages metabolites analysis. Results Arg-1, IL-10, CD163, CD206, and CRNDE were significantly up-regulated in HCC tissues, M2 macrophage and M0 macrophage with CRNDE overexpressed (OV-CRNDE-M0), which downregulated in M0 macrophage with CRNDE knockdown (sh-CRNDE-M0). The conditioned medium (CM) of M2 cells and OV-CRNDE-M0 cells promoted cell viability, invasion, and migration of HCC cells, the effect was reversed by sh-CRNDE-M0 cells CM. OV-CRNDE-M0 cells promoted tumor growth, Ki67 and CD206 expression in xenograft model. 61 metabolites were detected, of which 18 metabolites changed significantly in OV-CRNDE-M0 group compared to M0 group, with 9 upregulated and 9 downregulated. KEGG analysis showed the enrichment pathways were biosynthesis, glyoxylate and dicarboxylate metabolism. SMPDB analysis showed the enrichment pathways were hypoacetylaspartia, canavan disease, and aspartate metabolism. Conclusion CRNDE regulated the metabolic reprogramming of M2 macrophage via ERK pathway, which thereby contributed to HCC proliferation, migration, and invasion.

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Emerging roles of non-coding RNAs in the metabolic reprogramming of tumor-associated macrophages

Cited by 8 publications

References 105 publications

Metabolic reprogramming by miRNAs in the tumor microenvironment: Focused on immunometabolism

Metabolic reprogramming by miRNAs in the tumor microenvironment: Focused on immunometabolism

Non-Coding RNAs in the Crosstalk between Breast Cancer Cells and Tumor-Associated Macrophages

LncRNA CRNDE promotes hepatoma cell proliferation by regulating the metabolic reprogramming of M2 macrophages via ERK pathway

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