HDAC1 mediates epithelial–mesenchymal transition and promotes cancer cell invasion in glioblastoma

Cheng, Zhe; Li, Suwen; Yuan, Jiaqi; Cheng, Shan; Huang, Shilu; Dong, Jun

doi:10.1016/j.prp.2023.154481

Cited by 11 publications

(2 citation statements)

References 32 publications

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“…Among them, high expression of HDAC1, CASP3, REST, HMG20B, FZD7, GNAI3, FZD1 and EPHB4 were associated with worse OS, DSS and PFI, while high expression of KCNJ9 and SCRT1 suggested better OS, DSS and PFI. Consistent with our results, high expression of HDAC1, CASP3, REST, GNAI3, FZD1, EPHB4 was found to correlate with poor prognosis of glioma, and inhibitors of HDAC1 inhibited the EMT process in glioma cells thereby affecting cell migration and invasion (57)(58)(59)(60)(61)(62). FZD7, linked to glioma cell motility and invasiveness, aligns with our observation of TGIF2 promoting glioma cell migration (63).…”

Section: Discussionsupporting

confidence: 90%

TGIF2 is a potential biomarker for diagnosis and prognosis of glioma

Zhang,

Dong

et al. 2024

Front. Immunol.

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BackgroundTGFB-induced factor homeobox 2 (TGIF2), a member of the Three-Amino-acid-Loop-Extension (TALE) superfamily, has been implicated in various malignant tumors. However, its prognostic significance in glioma, impact on tumor immune infiltration, and underlying mechanisms in glioma development remain elusive.MethodsThe expression of TGIF2 in various human normal tissues, normal brain tissues, and gliomas was investigated using HPA, TCGA, GTEx, and GEO databases. The study employed several approaches, including Kaplan-Meier analysis, ROC analysis, logistic regression, Cox regression, GO analysis, KEGG analysis, and GSEA, to explore the relationship between TGIF2 expression and clinicopathologic features, prognostic value, and potential biological functions in glioma patients. The impact of TGIF2 on tumor immune infiltration was assessed through Estimate, ssGSEA, and Spearman analysis. Genes coexpressed with TGIF2 were identified, and the protein-protein interaction (PPI) network of these coexpressed genes were constructed using the STRING database and Cytoscape software. Hub genes were identified using CytoHubba plugin, and their clinical predictive value was explored. Furthermore, in vitro experiments were performed by knocking down and knocking out TGIF2 using siRNA and CRISPR/Cas9 gene editing, and the role of TGIF2 in glioma cell invasion and migration was analyzed using transwell assay, scratch wound-healing assay, RT-qPCR, and Western blot.ResultsTGIF2 mRNA was found to be upregulated in 21 cancers, including glioma. High expression of TGIF2 was associated with malignant phenotypes and poor prognosis in glioma patients, indicating its potential as an independent prognostic factor. Furthermore, elevated TGIF2 expression positively correlated with cell cycle regulation, DNA synthesis and repair, extracellular matrix (ECM) components, immune response, and several signaling pathways that promote tumor progression. TGIF2 showed correlations with Th2 cells, macrophages, and various immunoregulatory genes. The hub genes coexpressed with TGIF2 demonstrated significant predictive value. Additionally, in vitro experiments revealed that knockdown and knockout of TGIF2 inhibited glioma cell invasion, migration and suppressed the epithelial-mesenchymal transition (EMT) phenotype.ConclusionTGIF2 emerges as a potential biomarker for glioma, possibly linked to tumor immune infiltration and EMT.

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Section: Discussionsupporting

confidence: 90%

TGIF2 is a potential biomarker for diagnosis and prognosis of glioma

Zhang,

Dong

et al. 2024

Front. Immunol.

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“…Another study also supported the pro-tumorigenic activity of HDAC1 and demonstrated its implication in epithelialmesenchymal transition and cell invasion. Functional enrichment analysis is also associated with HDAC1 overexpression and regulation of critical cellular pathways such as glycolysis, hypoxia, and inflammation [81].…”

Section: Regulation Of Histone Acetyltransferases and Deacetylases By...mentioning

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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Epigenetic regulation in cancer therapy: From mechanisms to clinical advances

Tao,

Zhou,

Luo

et al. 2024

MedComm – Oncology

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Epigenetic regulation refers to the alteration of gene expression independent of changes in DNA sequence. It involves chemical modifications such as DNA methylation, histone methylation, and histone acetylation, which are regulated by a coordinated interplay of various regulators to ensure precise spatial and temporal regulation of gene expression. Epigenetic aberrations are commonly observed in cancer and are considered as hallmarks of cancer. In recent years, small molecules targeting specific epigenetic regulators have been developed and are demonstrating promising therapeutic potential in preclinical and clinical trials for cancer treatment. In this review, we summarize the essential regulatory mechanisms and dysfunctions of epigenetic regulators involved in DNA methylation, histone methylation, and histone acetylation during tumor development and progression. Moreover, we discuss the current advances and challenges in cancer epigenetic therapy that target these mechanisms in both hematologic malignancies and solid tumors. Finally, we discuss the potential of combining epigenetic drugs with other therapies, including chemotherapy, radiotherapy, targeted therapy, and immunotherapy, as a promising approach for cancer treatment. Overall, we aim to enhance the understanding of epigenetic regulation in cancer therapy and explore targeted therapeutic strategies based on these mechanisms, to ultimately advance cancer therapy and improve patient prognosis.

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HDAC1 mediates epithelial–mesenchymal transition and promotes cancer cell invasion in glioblastoma

Cited by 11 publications

References 32 publications

TGIF2 is a potential biomarker for diagnosis and prognosis of glioma

TGIF2 is a potential biomarker for diagnosis and prognosis of glioma

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

Epigenetic regulation in cancer therapy: From mechanisms to clinical advances

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