Methylation of SFRPs and APC Genes in Ovarian Cancer Infected with High Risk Human Papillomavirus

Al‐Shabanah, Othman A.; Hafez, Mohamed M.; Hassan, Zeinab K.; Sayed‐Ahmed, Mohamed M.; Abozeed, Waleed; Alsheikh, Abdulmalik; Al-Rejaie, Salem S.

doi:10.7314/apjcp.2014.15.6.2719

Cited by 18 publications

(17 citation statements)

References 64 publications

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“…In cervical cancer, HPV DNA integration in the host genome, genomic rearrangement, involving structural changes at the HPV DNA integration site, and the activation of replication at viral integrated sequences contribute to oncogenesis [121][122][123]. Genetic alterations which foster carcinogenesis involve DNA methylation and nucleotide polymorphisms.…”

Section: The Role Of Human Papillomavirus In Oncogenesismentioning

confidence: 99%

“…Genetic alterations which foster carcinogenesis involve DNA methylation and nucleotide polymorphisms. HPV-mediated promoter hypermethylation of tumor-suppressor genes, such as cell adhesion molecule 1 (CADM1), myelin and lymphocyte protein (MAL), paired box 1 (PAX1), adenylate cyclase activating polypeptide 1 (ADCYAP1), secreted frizzled-related protein (SFRP) and adenomatous polyposis coli, may have implications in the development of OC [71,121].…”

Section: The Role Of Human Papillomavirus In Oncogenesismentioning

confidence: 99%

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Factors in Oncogenesis: Viral Infections in Ovarian Cancer

Wilczyński

Paradowska

2020

Cancers

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Ovarian cancer (OC) is one of the leading causes of cancer death in women, with high-grade serous ovarian cancer (HGSOC) being the most lethal gynecologic malignancy among women. This high fatality rate is the result of diagnosis of a high number of new cases when cancer implants have already spread. The poor prognosis is due to our inadequate understanding of the molecular mechanisms preceding ovarian malignancy. Knowledge about the site of origination has been improved recently by the discovery of tube intraepithelial cancer (TIC), but the potential risk factors are still obscure. Due to high tumoral heterogeneity in OC, the establishment of early stage biomarkers is still underway. Microbial infection may induce or result in chronic inflammatory infection and in the pathogenesis of cancers. Microbiome research has shed light on the relationships between the host and microbiota, as well as the direct roles of host pathogens in cancer development, progression, and drug efficacy. While controversial, the detection of viruses within ovarian malignancies and fallopian tube tissues suggests that these pathogens may play a role in the development of OC. Genomic and proteomic approaches have enhanced the methods for identifying candidates in early screening. This article summarizes the existing knowledge related to the molecular mechanisms that lead to tumorigenesis in the ovary, as well as the viruses detected in OC cases and how they may elevate this process.

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Section: The Role Of Human Papillomavirus In Oncogenesismentioning

confidence: 99%

Section: The Role Of Human Papillomavirus In Oncogenesismentioning

confidence: 99%

Factors in Oncogenesis: Viral Infections in Ovarian Cancer

Wilczyński

Paradowska

2020

Cancers

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“…Epigenetic changes that suppress the activity of the negative regulator of the Wnt pathway have also been identified. Specifically, methylation markers in the APC and SFRP3 promoters have been found in ovarian cancer samples, but only in cases in which HR-HPV genomic sequences were detected [ 129 ]. Moreover, in cervical cancer samples, methylation markers have been found in the SRFP2 and DKK3 promoters [ 130 ].…”

Section: Wnt/β-catenin Signaling In Hpv-related Cancersmentioning

confidence: 99%

Regulation of the Wnt/β-Catenin Signaling Pathway by Human Papillomavirus E6 and E7 Oncoproteins

Muñoz-Bello

Nieva

Paredes

et al. 2015

Viruses

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Cell signaling pathways are the mechanisms by which cells transduce external stimuli, which control the transcription of genes, to regulate diverse biological effects. In cancer, distinct signaling pathways, such as the Wnt/β-catenin pathway, have been implicated in the deregulation of critical molecular processes that affect cell proliferation and differentiation. For example, changes in β-catenin localization have been identified in Human Papillomavirus (HPV)-related cancers as the lesion progresses. Specifically, β-catenin relocates from the membrane/cytoplasm to the nucleus, suggesting that this transcription regulator participates in cervical carcinogenesis. The E6 and E7 oncoproteins are responsible for the transforming activity of HPV, and some studies have implicated these viral oncoproteins in the regulation of the Wnt/β-catenin pathway. Nevertheless, new interactions of HPV oncoproteins with cellular proteins are emerging, and the study of the biological effects of such interactions will help to understand HPV-related carcinogenesis. This review addresses the accumulated evidence of the involvement of the HPV E6 and E7 oncoproteins in the activation of the Wnt/β-catenin pathway.

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“…A previous study showed that new tumor suppressors, such as the secreted frizzled-related protein (SFRP) gene, exhibited higher levels of methylation in the HPV-positive than in the HPV-negative group in ovarian cancer, and that the increase in the methylation pattern of the SFRP1 gene might be due to viral infection and integration into host cells ( 31 ). Some authors have also suggested that HPV interferes with the cellular DNA methylation machinery, either to conceal itself or as part of its viral cycle ( 32 ).…”

Section: Discussionmentioning

confidence: 99%

Hypermethylation of the tumor-suppressor cell adhesion molecule 1 in human papillomavirus-transformed cervical carcinoma cells

Woo

Kim

Song

et al. 2015

International Journal of Oncology

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Epigenetic modification at CpG islands located on the promoter regions of tumor-suppressor genes has been associated with tumor development in many human cancers. Our study showed that the cell adhesion molecule 1 (CADM1) is downregulated in human papillomavirus (HPV)-infected cervical cancer cell lines via its hypermethylation and demethylation using 5-aza-2′-deoxycyticine (5-aza-dC) restored the expression of CADM1 protein. Overexpression of CADM1 inhibited cell proliferation. p53 was involved in the regulation of CADM1. Our results demonstrate that epigenetic alteration of CADM1 was more frequent in HPV-positive cervical cancers and that restoration of CADM1 expression may be a potential strategy for cervical cancer therapy.

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Methylation of SFRPs and APC Genes in Ovarian Cancer Infected with High Risk Human Papillomavirus

Cited by 18 publications

References 64 publications

Factors in Oncogenesis: Viral Infections in Ovarian Cancer

Factors in Oncogenesis: Viral Infections in Ovarian Cancer

Regulation of the Wnt/β-Catenin Signaling Pathway by Human Papillomavirus E6 and E7 Oncoproteins

Hypermethylation of the tumor-suppressor cell adhesion molecule 1 in human papillomavirus-transformed cervical carcinoma cells

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