Asymmetric dimethylation at histone H3 arginine 2 by PRMT6 in gastric cancer progression

Okuno, Keisuke; Akiyama, Yoshimitsu; Shimada, Shu; Nakagawa, Masatoshi; Tanioka, Toshiro; Inokuchi, Mikito; Shoji, Yasuhiro; Kojima, Kazuyuki; Tanaka, Shinji

doi:10.1093/carcin/bgy147

Cited by 29 publications

(22 citation statements)

References 51 publications

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“…However, in gastric cancer, the knockout of tumor suppressor gene PCDH7 in PRMT6-KO-GC cells promotes cell migration and invasion. Gastric cancer cells overexpressing PRMT6 may increase invasiveness by directly repressing PCDH7 by increasing the H3R2me2as level (51). In androgen-independent prostate cancer (AIPC), androgen receptor targets PCDH7, and its hypermethylation may inhibit the growth and invasion of AIPC cells and promote apoptosis.…”

Section: Discussionmentioning

confidence: 99%

The predictive prognostic values of CBFA2T3, STX3, DENR, EGLN1, FUT4, and PCDH7 in lung cancer

et al. 2021

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Background: Lung cancer is one of the most malignant tumors. However, neither the pathogenesis of lung cancer nor the prognosis markers are completely clear. The purpose of this study is to screen the diagnostic or prognostic markers of lung cancer.Methods: TCGA and GEO datasets were used to analyze the relationship between lung cancer-related genes and lung cancer samples. Common differential genes were screened, and a univariate Cox regression analysis was used to screen survival related genes. A univariable Cox proportional hazards regression analysis was used to verify the genes and construct risk model. The key factors affecting the prognosis of lung cancer were determined by univariate and multivariate regression analyses. The ROC curve, AUC and the survival of each risk gene was analyzed. Finally, the biological functions of high-and low-risk patients were explored by GSEA and an immune-infiltration analysis.Results: Based on the common differential genes, 13 genes significantly related to lung cancer survival were identified. Eight risk genes (CBFA2T3, DENR, EGLN1, FUT2, FUT4, PCDH7, PHF14, and STX3) were screened out. The results showed that risk status may be an independent prognostic factor, and the risk score predicted the prognosis of lung cancer. CBFA2T3 and STX3 are protective genes, while DENR, EGLN1, FUT4 and PCDH7 are dangerous genes. These 6 genes can be used as independent lung cancer prognosis markers. The corresponding biological functions of genes expressed in high-risk patients were mostly related to tumor proliferation and inflammatory infiltration. Neutrophil, CD8 + T, Macrophage M0, Macrophage M1-and mDC-activated cells were high in high-risk status samples.Conclusions: CBFA2T3, STX3, DENR, EGLN1, FUT4, and PCDH7 are important participants in the occurrence and development of lung cancer. High-risk patients display serious inflammatory infiltration.This study not only provides insight into the mechanism of occurrence and development of lung cancer, but also provides potential targets for targeted therapy of lung cancer.

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Section: Discussionmentioning

confidence: 99%

The predictive prognostic values of CBFA2T3, STX3, DENR, EGLN1, FUT4, and PCDH7 in lung cancer

et al. 2021

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“…Aberrant expression of PRMT6 widely exists in cancers like lung (Avasarala et al, 2020), liver (Chan et al, 2018), gastric (Okuno et al, 2019), and prostate (Vieira et al, 2014) cancer and viral infections (Zhang et al, 2019). However, the modulation of PRMT6 protein has not been elucidated.…”

Section: Discussionmentioning

confidence: 99%

F-Box Protein FBXW17-Mediated Proteasomal Degradation of Protein Methyltransferase PRMT6 Exaggerates CSE-Induced Lung Epithelial Inflammation and Apoptosis

Luo

et al. 2021

Front. Cell Dev. Biol.

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Chronic obstructive pulmonary disease (COPD) is a chronic debilitating lung disease, characterized by progressive airway inflammation and lung structural cell death. Cigarette smoke is considered the most common risk factor of COPD pathogenesis. Understanding the molecular mechanisms of persistent inflammation and epithelial apoptosis induced by cigarette smoke would be extremely beneficial for improving the treatment and prevention of COPD. A histone methyl modifier, protein arginine N-methyltransferase 6 (PRMT6), is reported to alleviate cigarette smoke extract (CSE)-induced emphysema through inhibiting inflammation and cell apoptosis. However, few studies have focused on the modulation of PRMT6 in regulating inflammation and cell apoptosis. In this study, we showed that protein expression of PRMT6 was aberrantly decreased in the lung tissue of COPD patients and CSE-treated epithelial cells. FBXW17, a member of the Skp1-Cullin-F-box (SCF) family of E3 ubiquitin ligases, selectively bound to PRMT6 in nuclei to modulate its elimination in the proteasome system. Proteasome inhibitor or silencing of FBXW17 abrogated CSE-induced PRMT6 protein degradation. Furthermore, negative alteration of FBXW17/PRMT6 signaling lessened the proapoptotic and proinflammatory effects of CSE in lung epithelial cells. Our study, therefore, provides a potential therapeutic target against the airway inflammation and cell death in CS-induced COPD.

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“…178 Moreover, PRMT6-overexpressing GC cells also acquire invasiveness through direct transcriptional inhibition of PCDH7 by increasing H3R2me2as level. 179 Another study conducted by Li et al demonstrated that H3K27me3 and H3K9me2, mediated directly and indirectly by EZH2, are enriched in the miR-218-2 promoter, thus leading to downregulation of gene expression in PC. Loss of miR-218 increases invasion and migration through the effect of the UDP-glycosyltransferase 8 (UGT8) protein.…”

Section: Invasion and Migrationmentioning

confidence: 99%

The role of histone methylation in the development of digestive cancers: a potential direction for cancer management

Chen

Ren

Yang

et al. 2020

Sig Transduct Target Ther

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Digestive cancers are the leading cause of cancer-related death worldwide and have high risks of morbidity and mortality. Histone methylation, which is mediated mainly by lysine methyltransferases, lysine demethylases, and protein arginine methyltransferases, has emerged as an essential mechanism regulating pathological processes in digestive cancers. Under certain conditions, aberrant expression of these modifiers leads to abnormal histone methylation or demethylation in the corresponding cancer-related genes, which contributes to different processes and phenotypes, such as carcinogenesis, proliferation, metabolic reprogramming, epithelial-mesenchymal transition, invasion, and migration, during digestive cancer development. In this review, we focus on the association between histone methylation regulation and the development of digestive cancers, including gastric cancer, liver cancer, pancreatic cancer, and colorectal cancer, as well as on its clinical application prospects, aiming to provide a new perspective on the management of digestive cancers.

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Asymmetric dimethylation at histone H3 arginine 2 by PRMT6 in gastric cancer progression

Cited by 29 publications

References 51 publications

The predictive prognostic values of CBFA2T3, STX3, DENR, EGLN1, FUT4, and PCDH7 in lung cancer

The predictive prognostic values of CBFA2T3, STX3, DENR, EGLN1, FUT4, and PCDH7 in lung cancer

F-Box Protein FBXW17-Mediated Proteasomal Degradation of Protein Methyltransferase PRMT6 Exaggerates CSE-Induced Lung Epithelial Inflammation and Apoptosis

The role of histone methylation in the development of digestive cancers: a potential direction for cancer management

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