Associations of P16INK4a promoter hypermethylation with squamous intra-epithelial lesion, cervical cancer and their clinicopathological features: a meta-analysis

Han, Ya‐di; Wang, Xuebin; Cui, Naiqiang; Zhang, Shuai; Wang, Chen; Zheng, Fang

doi:10.18632/oncotarget.12202

Cited by 12 publications

(8 citation statements)

References 64 publications

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“…It has been found that during the development of carcinomas, including various stages of cervical cancer, numerous epigenetic changes, such as hyperand hypomethylation of DNA and tumor suppressor genes and modification of histones associated with the promoter regions of regulatory genes are observed. The results of meta-analysis confirm the hypermethylation of p16INK4a as an epigenetic marker for the progression of carcinogenesis in cervical cancer [65]. Expression of tumor suppressor genes, oncogenes, and growth factors is regulated by many histone-modifying enzymes, such as deacetylases and histone acetyltransferases; changes in the expression of histone modifiers also lead to epigenetic control of gene expression [16].…”

Section: Mechanisms Of Cervical Carcinogenesismentioning

confidence: 67%

“…According to different research, in HPV infection and cervical cancer there are various epigenetic changes and DNA methylation processes, and the participation of microRNAs in these processes has been described [18,19,65,83,[85][86][87][88]. At present, many of these processes have been studied insufficiently, and their interpretation is ambiguous, so the molecular mechanisms underlying these pathological changes are being investigated [11,14,85].…”

Section: Mechanisms Of Cervical Carcinogenesismentioning

confidence: 99%

“…Angiogenesis is stimulated by angiogenic factors, which are prognostic and predictive, the main ones being vascular endothelial growth factor (VEGF), fibroblast growth factor (FGF), angiogenin, transforming growth factor-α (TGF-α). VEGF is an important mediator of neoangiogenesis, stimulating the proliferation of endothelial cells and enhancing vascular permeability, as well as indirectly affecting lymphangiogenesis; VEGF is an important therapeutic target in the development of antiangiogenic anticancer drugs [65,66]. To assess angiogenesis in tumors, antibodies to endothelial cell markers-factor VIII, CD31, CD34, and others-are used.…”

Section: Markers Of Angiogenesis In Cervical Carcinogenesismentioning

confidence: 99%

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Cervical Carcinoma: Oncobiology and Biomarkers

Volkova

Pashov

Omelchuk

2021

IJMS

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Cervical cancer is one of the most common types of carcinomas causing morbidity and mortality in women in all countries of the world. At the moment, the oncology, oncobiology, and oncomorphology of cervical cancer are characterized by the accumulation of new information; various molecular biological, genetic, and immunohistochemical methods of investigation of the mechanisms of cervical carcinogenesis are tested and applied; targeted antitumour drugs and diagnostic, prognostic, and predictive biomarkers are being searched for. Many issues of the etiopathogenesis of cervical cancer have not been sufficiently studied, and the role of many biomarkers characterizing various stages of cervical carcinogenesis remains unclear. Therefore, the target of this review is to systematize and understand several problems in the pathogenesis of cervical cancer and to evaluate the significance and role of biomarkers in cervical carcinogenesis.

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Section: Mechanisms Of Cervical Carcinogenesismentioning

confidence: 67%

Section: Mechanisms Of Cervical Carcinogenesismentioning

confidence: 99%

Section: Markers Of Angiogenesis In Cervical Carcinogenesismentioning

confidence: 99%

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Cervical Carcinoma: Oncobiology and Biomarkers

Volkova

Pashov

Omelchuk

2021

IJMS

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“…The promoter regions of p16 are often methylated, which decreases the levels of p16 in cervical cancer (8). Previous studies have demonstrated that p16 promoter methylation is closely associated with the development and progression of cervical cancer, so it is considered a potential diagnostic and therapeutic target (9,10). The changes involved in DNA methylation are controlled by DNA methyltransferases (DNMTs) (11).…”

Section: Introductionmentioning

confidence: 99%

MicroRNA‑29a inhibits cell proliferation and arrests cell cycle by modulating p16 methylation in cervical cancer

Wang

Rengaowa

et al. 2021

Oncol Lett

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Cervical cancer is the second most common gynecological malignancy. Accumulating evidence has suggested that microRNAs (miRNAs) are involved in the occurrence and development of cervical cancer. The present study aimed to investigate the function and underlying molecular mechanism of microRNA (miRNA/miR)-29a in cervical cancer. Reverse transcription-quantitative PCR and methylation-specific PCR were used to examine the expression of miR-29a and methylated status of p16 promoter, respectively. Cell Counting Kit-8 analysis and flow cytometry were performed to evaluate cell viability and cycle, respectively. Dual-luciferase reporter assay was performed to verify the interaction between miR-29a and its targets. Western blot analysis was performed to detect the protein levels of DNA methyltransferases (DNMT)3A and DNMT3B. The results demonstrated that miR-29a expression was downregulated in cervical cancer tissues and cells, and negatively correlated with p16 promoter hypermethylation. Furthermore, cell experiments confirmed that miR-29a suppressed cell proliferation and induced cell cycle arrest in HeLa and C-33A cells. Mechanically, miR-29a restored normal methylation pattern of the p16 gene by sponging DNMT3A and DNMT3B. Taken together, the results of the present study demonstrated the epigenetic regulation of tumor suppressor p16 by miR-29a as a unique mechanism, thus providing a rationale for the development of miRNA-based strategies in the treatment of cervical cancer.

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“…The imprint and non-imprint methylation marks at these DMRs are established during gametogenesis and affected by environmental exposures (Li et al, 2016). P16 methylation is strongly associated with smoking in different pathological conditions, including lung cancer and cervical cancer (Han et al, 2016; Han et al, 2017; Wang et al, 2017). However, the relationship between these genes, tobacco/alcohol exposure, and male infertility has not yet been elucidated.…”

Section: Introductionmentioning

confidence: 99%

Association of Sperm Methylation at LINE-1, Four Candidate Genes, and Nicotine/Alcohol Exposure With the Risk of Infertility

Zhang

Sun

et al. 2019

Front. Genet.

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In this study, we examined whether smoking and drinking affect sperm quality and the DNA methylation of the repetitive element LINE-1, MEST, P16, H19, and GNAS in sperm. Semen samples were obtained from 143 male residents in a minority-inhabited district of Guizhou province in southwest China. Quantitative DNA methylation analysis of the samples was performed using MassARRAY EpiTYPER assays. Sperm motility was significantly lower in both the nicotine-exposed (P = 0.0064) and the nicotine- and alcohol-exposed (P = 0.0008) groups. Follicle-stimulating hormone (FSH) levels were higher in the nicotine-exposed group (P = 0.0026). The repetitive element LINE-1 was hypermethylated in the three exposed groups, while P16 was hypomethylated in the alcohol and both the alcohol and nicotine exposure groups. Our results also show that alcohol and nicotine exposure altered sperm cell quality, which may be related to the methylation levels of MEST and GNAS. In addition, MEST, GNAS, and the repetitive element LINE1 methylation was significantly associated with the concentration of sperm as well as FSH and luteinizing hormone levels.

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Associations of P16INK4a promoter hypermethylation with squamous intra-epithelial lesion, cervical cancer and their clinicopathological features: a meta-analysis

Abstract: ABSTRACT

Cited by 12 publications

References 64 publications

Cervical Carcinoma: Oncobiology and Biomarkers

Cervical Carcinoma: Oncobiology and Biomarkers

MicroRNA‑29a inhibits cell proliferation and arrests cell cycle by modulating p16 methylation in cervical cancer

Association of Sperm Methylation at LINE-1, Four Candidate Genes, and Nicotine/Alcohol Exposure With the Risk of Infertility

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