Dual role of pseudogene TMEM198B in promoting lipid metabolism and immune escape of glioma cells

Zhan, Yong; Qiao, Wei; Yi, Bolong; Yang, Xinyu; Li, Miaomiao; Sun, Lu; Ji, Lian; Su, Peng; Wang, Xin; Zhang, Furong; Zhang, Rui; Gao, Mingjun; Zhao, Wujun; Song, Yichen

doi:10.1038/s41388-022-02445-0

Cited by 12 publications

(13 citation statements)

References 44 publications

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“…Given the critical roles of PLAGL2 in tumorigenesis, the mechanisms contributing to PLAGL2 expression are investigated by numerous studies. For example, the previous studies have shown that PLAGL2 was targeted by non‐coding RNAs, like miR‐22‐3p in breast cancer, 22 miR‐128‐3p in multiple myeloma, 23 and pseudogene TMEM198B in glioma 24 . Additionally, GATA binding protein 5 (GATA5) is shown to regulate PLAGL2 expression through the FAK/PI3K/AKT pathway and thus suppress prostate cancer progression 13 .…”

Section: Discussionmentioning

confidence: 99%

“…For example, the previous studies have shown that PLAGL2 was targeted by non-coding RNAs, like miR-22-3p in breast cancer, 22 miR-128-3p in multiple myeloma, 23 and pseudogene TMEM198B in glioma. 24 Additionally, GATA binding protein 5 (GATA5) is shown to regulate PLAGL2 expression through the FAK/PI3K/AKT pathway and thus suppress prostate cancer progression. 13 But the precise mechanism controlling PLAGL2 expression in lung cancer was unknown.…”

Section: Discussionmentioning

confidence: 99%

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PLAGL2 promotes the stemness and is upregulated by transcription factor E2F1 in human lung cancer

Yuan

Lin²,

Guo

et al. 2023

Environmental Toxicology

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This study mainly focuses on revealing the role of PLAGL2 in lung cancer stemness.In vitro and in vivo experiments were performed to evaluate the effects of PLAGL2 on lung cancer cell stemness. Mechanistic analysis using luciferase reporter and ChIP assays were implemented to reveal the underlying mechanisms. The transcriptional factor E2F1 transcriptionally activated PLAGL2 expression via directly binding to PLAGL2 promoter in lung cancer cells. Moreover, PLAGL2 promoted the stemness of lung cancer cells dependent on E2F1-mediated transcriptional activation. This study provides a potential target for lung cancer progression.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

PLAGL2 promotes the stemness and is upregulated by transcription factor E2F1 in human lung cancer

Yuan

Lin²,

Guo

et al. 2023

Environmental Toxicology

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“…M1-like macrophages can produce tumor necrosis factors, inflammatory cytokines, and reactive oxygen species, which can promote inflammatory reactions and eliminate tumor cells, while M2-like macrophages produce different cytokines from M1-like macrophages, such as tumor-stimulating cytokines, which can promote tumor angiogenesis and tumor proliferation, leading to immunosuppression ( 82 ). In addition, M2-like macrophages can also produce a variety of chemokines to affect other immune cells ( 83 ).…”

Section: Effect Of Metabolism On Immune Cellsmentioning

confidence: 99%

Analyzing the impact of metabolism on immune cells in tumor microenvironment to promote the development of immunotherapy

Long,

Shi,

et al. 2024

Front. Immunol.

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Tumor metabolism and tumor immunity are inextricably linked. Targeting the metabolism of tumors is a point worth studying in tumor immunotherapy. Recently, the influence of the metabolism of tumors and immune cells on the occurrence, proliferation, metastasis, and prognosis of tumors has attracted more attention. Tumor tissue forms a specific tumor microenvironment (TME). In addition to tumor cells, there are also immune cells, stromal cells, and other cells in TME. To adapt to the environment, tumor cells go through the metabolism reprogramming of various substances. The metabolism reprogramming of tumor cells may further affect the formation of the tumor microenvironment and the function of a variety of cells, especially immune cells, eventually promoting tumor development. Therefore, it is necessary to study the metabolism of tumor cells and its effects on immune cells to guide tumor immunotherapy. Inhibiting tumor metabolism may restore immune balance and promote the immune response in tumors. This article will describe glucose metabolism, lipid metabolism, amino acid metabolism, and immune cells in tumors. Besides, the impact of metabolism on the immune cells in TME is also discussed for analyzing and exploring tumor immunotherapy.

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“…TMEM198B is highly expressed in glioma tissues and cell lines and mediates trimethylation on H3K4me3 by binding to the SET structural domain of SETD1B, thereby promoting the expression of PLAGL2. Moreover, TMEM198B is enriched in glioma‐derived exosomes (GDEs) and can be delivered to macrophages and enhance lipid accumulation and fatty acid oxidation (FAO), further inducing macrophages to polarize toward M2, thereby promoting immune escape of glioma cells 69 …”

Section: Characteristics Of the Components Of The Glioma Immune Micro...mentioning

confidence: 99%

Advances in research on immune escape mechanism of glioma

Guo

Wang

2023

CNS Neurosci Ther

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Background Glioma is the most common primary intracranial malignancy in clinical practice, and in particular, IDH‐wildtype glioblastoma has the worst prognosis. In recent years, surgical resection combined with simultaneous radiotherapy and immune checkpoint inhibitors has made some progress, but the efficacy is still not satisfactory, which may be related to the low immunogenicity of glioma cells and the tumor immunosuppressive microenvironment. Methods A comprehensive review of relevant literature was conducted to explore the mechanisms by which tumors suppress antitumor immune responses and produce escape, with a focus on the immune cells in the tumor microenvironment (TME). Results The mechanisms involved in immune evasion of glioma cells are complex and involve with immune cell differentiation and function. Conclusion Our review emphasizes the need for a more profound comprehension of the mechanisms involved in immune response and immune evasion in glioma, to formulate more efficacious treatment modalities.

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Dual role of pseudogene TMEM198B in promoting lipid metabolism and immune escape of glioma cells

Cited by 12 publications

References 44 publications

PLAGL2 promotes the stemness and is upregulated by transcription factor E2F1 in human lung cancer

PLAGL2 promotes the stemness and is upregulated by transcription factor E2F1 in human lung cancer

Analyzing the impact of metabolism on immune cells in tumor microenvironment to promote the development of immunotherapy

Advances in research on immune escape mechanism of glioma

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