Homeobox genes gain trimethylation of histone H3 lysine 4 in glioblastoma tissue

Luo, Kun; Luo, Da; Wen, Hao

doi:10.1042/bsr20160028

Cited by 4 publications

(6 citation statements)

References 36 publications

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“…As research has progressed, the genomic landscape of cancer has been gradually brought into light, and an increasing number of vital genes shared by various cancers [28,29], ERCC4/XPF for example, have been revealed in recent years. The XPF-rs2276466 polymorphism was widely reported to be associated with susceptibility of a wide range of cancers [30].…”

Section: Discussionmentioning

confidence: 99%

Impact of XPF rs2276466 polymorphism on cancer susceptibility: a meta-analysis

Liu

Liu²,

Zhao

et al. 2019

Bioscience Reports

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Association between the xeroderma pigmentosum complementation group F (XPF)rs2276466 located in the excision repair cross complementation group 4 (ERCC4) gene and cancer susceptibility has been widely investigated. However, results thus far have remained controversial. A meta-analysis was performed to identify the impact of this polymorphism on cancer susceptibility. PubMed, Embase and Science-Web databases were searched systematically up to May 20, 2018, to obtain all the records evaluating the association between the rs2276466 polymorphism and the risk of all types of cancers. We used the odds ratio (OR) as a measure of effect, and pooled the data in a Mantel-Haenszel weighed random-effects meta-analysis to provide a summary estimate of the impact of this polymorphism on gastrointestinal cancer, neurogenic cancer and other cancers (breast cancer and SCCHN). All the analyses were carried out in STATA 14.1.11 case–control studies that consisted of 5730 cases and 6756 controls, were eventually included in our meta-analysis. The significant association was observed between the XPFrs2276466 polymorphism and neurogenic cancer susceptibility (recessive model: OR = 1.648, 95% CI = 1.294–2.098, P<0.001). Furthermore, no significant impact of this polymorphism was detected on decreased gastrointestinal cancer risk (dominant model: OR = 1.064, 95%CI = 0.961–1.177, P = 0.233). The rs2276466 polymorphism might play different roles in carcinogenesis of various cancer types. Current evidence did not suggest that this polymorphism was directly associated with gastrointestinal susceptibility. However, this polymorphism might contribute to increased neurogenic cancer risk. More preclinical and epidemiological studies are still imperative for further evaluation

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Section: Discussionmentioning

confidence: 99%

Impact of XPF rs2276466 polymorphism on cancer susceptibility: a meta-analysis

Liu

Liu²,

Zhao

et al. 2019

Bioscience Reports

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“…186,187 The decrease of H3K4me3 content in the promoter was also detected. 188 Christina et al found that the changes in gene expression of various methyltransferases, acetyltransferases, and deacetylases promoted the pathogenesis of GBM. 189 The nuclear expression levels of lysine methyltransferases SETDB1, KMT5B, Suv-39h1, and EZH2 in GBM are upregulated, compared with normal tissues, and correlated with advanced histological grades.…”

Section: Glioblastoma (Gbm)mentioning

confidence: 99%

“…K27M mutation was found in 30% of children with high‐grade GBM, which was related to adverse clinical outcomes 186,187 . The decrease of H3K4me3 content in the promoter was also detected 188 . Christina et al.…”

Section: Abnormal Expression Of Histone‐modifying Enzymes and Human C...mentioning

confidence: 99%

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Post‐translational modifications of histones: Mechanisms, biological functions, and therapeutic targets

Liu

Guo

et al. 2023

MedComm

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Histones are DNA‐binding basic proteins found in chromosomes. After the histone translation, its amino tail undergoes various modifications, such as methylation, acetylation, phosphorylation, ubiquitination, malonylation, propionylation, butyrylation, crotonylation, and lactylation, which together constitute the “histone code.” The relationship between their combination and biological function can be used as an important epigenetic marker. Methylation and demethylation of the same histone residue, acetylation and deacetylation, phosphorylation and dephosphorylation, and even methylation and acetylation between different histone residues cooperate or antagonize with each other, forming a complex network. Histone‐modifying enzymes, which cause numerous histone codes, have become a hot topic in the research on cancer therapeutic targets. Therefore, a thorough understanding of the role of histone post‐translational modifications (PTMs) in cell life activities is very important for preventing and treating human diseases. In this review, several most thoroughly studied and newly discovered histone PTMs are introduced. Furthermore, we focus on the histone‐modifying enzymes with carcinogenic potential, their abnormal modification sites in various tumors, and multiple essential molecular regulation mechanism. Finally, we summarize the missing areas of the current research and point out the direction of future research. We hope to provide a comprehensive understanding and promote further research in this field.

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“…Studies have shown increased and decreased lysine 4 trimethylation levels of histone H3 (H3K4me3) in GBM compared to normal brain tissue [57,58]. These changes can affect the expression of genes involved in critical cellular processes, including cell cycle regulation, DNA repair, and tumor suppression.…”

Section: Histone Methyltransferases and Mirnasmentioning

confidence: 99%

The Role of Non-Coding RNAs in Epigenetic Dysregulation in Glioblastoma Development

Isachesku,

Braicu,

Pirlog

et al. 2023

IJMS

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Glioblastoma (GBM) is a primary brain tumor arising from glial cells. The tumor is highly aggressive, the reason for which it has become the deadliest brain tumor type with the poorest prognosis. Like other cancers, it compromises molecular alteration on genetic and epigenetic levels. Epigenetics refers to changes in gene expression or cellular phenotype without the occurrence of any genetic mutations or DNA sequence alterations in the driver tumor-related genes. These epigenetic changes are reversible, making them convenient targets in cancer therapy. Therefore, we aim to review critical epigenetic dysregulation processes in glioblastoma. We will highlight the significant affected tumor-related pathways and their outcomes, such as regulation of cell cycle progression, cell growth, apoptosis, angiogenesis, cell invasiveness, immune evasion, or acquirement of drug resistance. Examples of molecular changes induced by epigenetic modifications, such as DNA epigenetic alterations, histone post-translational modifications (PTMs), and non-coding RNA (ncRNA) regulation, are highlighted. As understanding the role of epigenetic regulators and underlying molecular mechanisms in the overall pro-tumorigenic landscape of glioblastoma is essential, this literature study will provide valuable insights for establishing the prognostic or diagnostic value of various non-coding transcripts, including miRNAs.

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Homeobox genes gain trimethylation of histone H3 lysine 4 in glioblastoma tissue

Abstract: We revealed that in GBM homeobox genes gain tri-methylation on lysine 4 of histone H3 (H3K4me3), whereas the cell–cell adhesion-related cadherin genes lose H3K4me3, suggesting that the H3K4me3 alteration is related to the formation and migration of GBM cells.

Cited by 4 publications

References 36 publications

Impact of XPF rs2276466 polymorphism on cancer susceptibility: a meta-analysis

Impact of XPF rs2276466 polymorphism on cancer susceptibility: a meta-analysis

Post‐translational modifications of histones: Mechanisms, biological functions, and therapeutic targets

The Role of Non-Coding RNAs in Epigenetic Dysregulation in Glioblastoma Development

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