Advances in epigenetic modifications and cervical cancer research

Liu, Hui; Ma, Hongbing; Li, Yang; Zhao, Hua

doi:10.1016/j.bbcan.2023.188894

Cited by 9 publications

(3 citation statements)

References 202 publications

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“…The development of cervical cancer is closely linked with chromatin modification, which exerts a crucial influence on gene expression and plays a pivotal role in the initiation and progression of tumors [ 4 , 5 ]. Among the various chromatin modifications, histone methylation on lysine residues has garnered significant attention and investigation [ 6 , 7 ].…”

Section: Introductionmentioning

confidence: 99%

Targeting histone demethylases JMJD3 and UTX: selenium as a potential therapeutic agent for cervical cancer

Chen,

Cai,

Zhu

et al. 2024

Clin Epigenet

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Background The intriguing connection between selenium and cancer resembles a captivating puzzle that keeps researchers engaged and curious. While selenium has shown promise in reducing cancer risks through supplementation, its interaction with epigenetics in cervical cancer remains a fascinating yet largely unexplored realm. Unraveling the intricacies of selenium's role and its interaction with epigenetic factors could unlock valuable insights in the battle against this complex disease. Result Selenium has shown remarkable inhibitory effects on cervical cancer cells in various ways. In in vitro studies, it effectively inhibits the proliferation, migration, and invasion of cervical cancer cells, while promoting apoptosis. Selenium also demonstrates significant inhibitory effects on human cervical cancer-derived organoids. Furthermore, in an in vivo study, the administration of selenium dioxide solution effectively suppresses the growth of cervical cancer tumors in mice. One of the mechanisms behind selenium's inhibitory effects is its ability to inhibit histone demethylases, specifically JMJD3 and UTX. This inhibition is observed both in vitro and in vivo. Notably, when JMJD3 and UTX are inhibited with GSK-J4, similar biological effects are observed in both in vitro and in vivo models, effectively inhibiting organoid models derived from cervical cancer patients. Inhibiting JMJD3 and UTX also induces G2/M phase arrest, promotes cellular apoptosis, and reverses epithelial-mesenchymal transition (EMT). ChIP-qPCR analysis confirms that JMJD3 and UTX inhibition increases the recruitment of a specific histone modification, H3K27me3, to the transcription start sites (TSS) of target genes in cervical cancer cells (HeLa and SiHa cells). Furthermore, the expressions of JMJD3 and UTX are found to be significantly higher in cervical cancer tissues compared to adjacent normal cervical tissues, suggesting their potential as therapeutic targets. Conclusions Our study highlights the significant inhibitory effects of selenium on the growth, migration, and invasion of cervical cancer cells, promoting apoptosis and displaying promising potential as a therapeutic agent. We identified the histone demethylases JMJD3 and UTX as specific targets of selenium, and their inhibition replicates the observed effects on cancer cell behavior. These findings suggest that JMJD3 and UTX could be valuable targets for selenium-based treatments of cervical cancer.

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Section: Introductionmentioning

confidence: 99%

Targeting histone demethylases JMJD3 and UTX: selenium as a potential therapeutic agent for cervical cancer

Chen,

Cai,

Zhu

et al. 2024

Clin Epigenet

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show abstract

“…When cervical cancer patients present with metastasis and recurrence, their prognosis is worse [ 9 ]. Therefore, based on its molecular mechanisms that remain to be elucidated, the search for new prognostic markers as well as the development of new therapeutic approaches is of great significance for cervical cancer [ 10 – 12 ].…”

Section: Introductionmentioning

confidence: 99%

DDOST is associated with tumor immunosuppressive microenvironment in cervical cancer

Mei,

Pan,

Huang

et al. 2024

Discov Onc

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Evidence has revealed that DDOST plays an important role in cancer development and progression. However, there are no reports on functions of DDOST in cervical tumorigenesis. Hence, we investigated the relationship of DDOST with prognosis, mutation, promoter methylation, immune cell infiltration, and drug sensitivity using bioinformatics techniques. Our results demonstrated that DDOST was significantly upregulated in a variety of tumor types and correlated with poor prognosis, including cervical cancer. Cox regression analysis dissected that high DDOST expression was associated with poor survival in cervical cancer patients. Immune infiltration analysis defined that DDOST was negatively correlated with CD8 T cells and NK cells. Strikingly, the sensitivity to multiple drugs was negatively correlated with the expression of DDOST. Therefore, our findings uncovered that DDOST could play an essential role in the tumor microenvironment and tumor immune regulation in cervical cancer, which indicated that DDOST could be a useful biomarker for prognosis and a potential therapeutic target for cancer treatment.

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“…One key focus of RNA methylation research is m6A, which regulates gene expression and plays a role in subsequent biological processes such as mRNA stability, transcription, and translation 7 , 8 . Abnormal regulation of RNA methylation has been associated with the development of tumors and age-related neurological diseases such as Alzheimer's disease 9 , Parkinson's disease 10 , and depression. Overall, epigenetics is a fascinating area of biology that is helping to illuminate the intricate ways that our genes are regulated and controlled.…”

Section: Introductionmentioning

confidence: 99%

A comprehensive epigenetic network can influence the occurrence of thyroid-associated ophthalmopathy by affecting immune and inflammatory response

Zhang,

Wu,

Gong

et al. 2024

Sci Rep

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The primary objective of this study is to understand the regulatory role of epigenetics in thyroid-associated ophthalmopathy (TAO) using multi-omics sequencing data. We utilized tRFs sequencing data, DNA methylation sequencing data, and lncRNA/circRNA/mRNA sequencing data, as well as several RNA methylation target prediction websites, to analyze the regulatory effect of DNA methylation, non-coding RNA, and RNA methylation on TAO-associated genes. Through differential expression analysis, we identified 1019 differentially expressed genes, 985 differentially methylated genes, and 2601 non-coding RNA. Functional analysis showed that differentially expressed genes were mostly associated with the PI3K signaling pathway and the IL17 signaling pathway. Genes regulated by DNA epigenetic regulatory networks were mainly related to the Cytokine-cytokine receptor interaction pathway, whereas genes regulated by RNA epigenetic regulatory networks were primarily related to the T cell receptor signaling pathway. Finally, our integrated regulatory network analysis revealed that epigenetics mainly impacts the occurrence of TAO through its effects on key pathways such as cell killing, cytokine production, and immune response. In summary, this study is the first to reveal a new mechanism underlying the development of TAO and provides new directions for future TAO research.

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Advances in epigenetic modifications and cervical cancer research

Cited by 9 publications

References 202 publications

Targeting histone demethylases JMJD3 and UTX: selenium as a potential therapeutic agent for cervical cancer

Targeting histone demethylases JMJD3 and UTX: selenium as a potential therapeutic agent for cervical cancer

DDOST is associated with tumor immunosuppressive microenvironment in cervical cancer

A comprehensive epigenetic network can influence the occurrence of thyroid-associated ophthalmopathy by affecting immune and inflammatory response

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