Silencing of histone deacetylase 2 suppresses malignancy for proliferation, migration, and invasion of glioblastoma cells and enhances temozolomide sensitivity

Zhang, Zhiqiang; Wang, Yunmin; Chen, Jiehan; Tan, Qijia; Xie, Caijun; Liu, Cong; Zhan, Wengang; Wang, Mei

doi:10.1007/s00280-016-3188-2

Cited by 45 publications

(37 citation statements)

References 24 publications

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“…High expression of HDAC2 has been reported in GBM cells [89]. Depletion of HDAC2 by siRNA suppresses proliferation, migration, and invasion of GBM cells and renders the cells sensitive to temozolomide.…”

Section: Preclinical Studies Of Hdacs and Hdac Inhibitors In Gbmmentioning

confidence: 99%

Advances in epigenetic glioblastoma therapy

et al. 2017

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Glioblastoma multiforme (GBM) is the most lethal primary brain tumor in adults despite contemporary gold-standard first-line treatment strategies. This type of tumor recurs in virtually all patients and no commonly accepted standard treatment exists for the recurrent disease. Therefore, advances in all scientific and clinical aspects of GBM are urgently needed. Epigenetic mechanisms are one of the major factors contributing to the pathogenesis of cancers, including glioblastoma. Epigenetic modulators that regulate gene expression by altering the epigenome and non-histone proteins are being exploited as therapeutic drug targets. Over the last decade, numerous preclinical and clinical studies on histone deacetylase (HDAC) inhibitors have shown promising results in various cancers. This article provides an overview of the anticancer mechanisms of HDAC inhibitors and the role of HDAC isoforms in GBM. We also summarize current knowledge on HDAC inhibitors on the basis of preclinical studies and emerging clinical data.

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Section: Preclinical Studies Of Hdacs and Hdac Inhibitors In Gbmmentioning

confidence: 99%

Advances in epigenetic glioblastoma therapy

et al. 2017

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“…Furthermore, there is a significant association of SIRT1 gene, a type II histone deacetylase and miR200a, key player in aging, obesity, and cancers; namely breast cancer. SIRT1 is also associated with the recruitment of DNMT (Peng et al, 2011) that hypermethylates promoter regions of tumour suppressor genes and enhances resistance to drugs (Wang and Chen, 2013;Zhang et al, 2016). This study revealed that TGFβ1 promotes EMT through overexpression of SIRT1, N-cadherin, and downregulation of E-cadherin in TGFβ-stimulated breast cancer cell (HME1).…”

Section: Histone Modificationsmentioning

confidence: 89%

Overview on Epigenetic Re-programming: A Potential Therapeutic Intervention in Triple Negative Breast Cancers

Hanif

Shah

2018

Asian Pac J Cancer Prev

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Cancer is one of the most common fatal diseases worldwide, and numbers have risen each year between 1971-2008 (National Cancer Statistics 2012). The International Agency for Research on Cancer (IARC), a specialized body of World Health Organization (WHO), reported 14.1 million new cancer cases and 8.2 million cancer-related deaths in 2012. According to IARC, the most common cancers worldwide were lung (13.0%), breast (11.9%), and colorectal (9.7%). Five-year survival was assessed in 32.6 million cancer cases in the same year, with highest fatalities reported in lung (19.4%), liver (9.1%) and stomach (8.8%) cancers (International Agency for Research on Cancer 2013). In Malaysia, breast cancer incidence is the highest, accounted for 17.7% among all other cancer cases. Breast cancer ranked top incidence in females, followed by cervix uteri, colorectal, ovarian and cancer of corpus uteri. Highest breast cancer incidence was seen in Malays encompassing 8,225 indicidence followed

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“…And it was a hub and potential driver gene in gliomas, its reported that it could activate PI3K/AKT and MEK/ERK signaling pathways to promote glioma cell proliferation and invasion and knockdown of it could induce glioma cell apoptosis and invasion suppression [34,40]. HDAC2 and HDAC3, both of which were upregulated with higher WHO grades, have been reported to be involved in glioma malignancy and chemoresistance [41][42][43]. The expression of HDAC7 is positively associated with a mesenchymal subtype of glioblastoma [44], and can enhance the malignant phenotype of glioma, while its inhibition may suppress STAT3 tumorigenic activity [45,46].…”

Section: Discussionmentioning

confidence: 99%

Multi-omics Prognostic Analysis of Lysine Acetylation Regulators in Glioma

et al. 2020

Preprint

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Background: Lysine acetylation is a crucial kind of protein modification and is related to the malignant development of various cancers. But their roles in glioma are still unclear and needed concluded comprehensively. Methods: In this study, we comprehensively analyzed the expression levels of 33 lysine acetylation regulators (LARs) and prognostic roles by using public data, including the Chinese Glioma Genome Atlas (CGGA) and The Cancer Genome Atlas (TCGA). The prognostic roles of LARs were judged by univariate Cox regression. Consensus clustering was applied to result in three stratified glioma subtypes (LA1, 2, and 3) with different clinical outcomes. We also constructed a risk signature for predicting the overall survival of glioma patients by using least absolute shrinkage and selection operator regression (LASSO regression). Besides, copy number variations (CNVs) and single nucleotide polymorphism (SNP) of LARs were also analyzed in our study. Results: We found the mRNA expression levels of most of LARs were dysregulated in gliomas and associated with the prognosis of glioma patients. The risk signature constructed by 14 LARs presented an independent prognostic role in both the CGGA (HR:1.96, 95%CI:1.33-2.90) and TCGA (HR:1.48, 95%CI:1.08-2.03) datasets and robust predictive effects in the ROC curves with all of area under curves more than 0.800. Moreover, the copy number variations of LARs were also significantly related to the prognosis of glioma patients, in which HDAC1 (1p) was one of the oncogenes lost in 1p/19q codeletion events, while SIRT2 (19q) and EP300 (22q) may act as tumor suppressors in gliomas with 19q or 22q deletions, respectively. Conclusion: LARs are potential biomarkers for the malignant progression of gliomas, and our results could be useful for predicting the OS of glioma patients and provide some clues in searching the functions of LARs in glioma progression. Keywords: glioma, lysine acetylation regulator, epigenetic, prognostic signature, biomarker.

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Silencing of histone deacetylase 2 suppresses malignancy for proliferation, migration, and invasion of glioblastoma cells and enhances temozolomide sensitivity

Cited by 45 publications

References 24 publications

Advances in epigenetic glioblastoma therapy

Advances in epigenetic glioblastoma therapy

Overview on Epigenetic Re-programming: A Potential Therapeutic Intervention in Triple Negative Breast Cancers

Multi-omics Prognostic Analysis of Lysine Acetylation Regulators in Glioma

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