Chapter 13, Epigenetic Mechanisms of Human Imprinting Disorders
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Selker 11 Epigenetics of Ciliates Douglas L. Kingston and John W. Becker and Jerry L. Kelly, Sevinc Ercan, and Jason D. Lucchesi and Mitzi I. Barlow and Marisa S. Zoghbi and Arthur L. Reports revealed that miRNAs encoded by viruses target host genes involved cell proliferation, apoptosis, host immunity regulation, in order to maintain their survival and to escape from immune system response.
Over miRNAs encoded by several virus families have been identified to date, many of them being found for herpes viruses and Epstein—Barr virus EBV [ ]. For instance, it was found that EBV encodes more than 40 miRNAs that presents different expression levels during viral infection and some are involved in maintaining viral latency [ , ]. Even though few lncRNAs have been well characterized, from the knowledge accumulated so far it is clear that they represent significant gene regulators and play critical roles in many cellular and development processes.
Therefore, taken into account, the wide functions that lncRNAs hold, it is not surprising that their alterations are associated with an extensive range of disease. Several studies have reported lncRNAs involvement in cardiovascular diseases, neurological disorders, immune disease, and also in cancer, data indicates a differential lncRNAs expression in many types of malignancy including, breast cancer, colon cancer, prostate cancer, hepatocellular carcinoma, pancreatic cancer, lymphomas [ ]. Currently, the expression profile of various ncRNAs has become an important feature of oncogenesis process.
There are numerous publications indicating an association between lncRNAs expression and malignant transformation and the number is still rising. Recently with the help of the latest NGS techniques, new information is brought to light for better understanding lncRNAs role, mechanisms of action, and also the potential use of them in various cancer therapies. Experimentally data sustain a potential oncogenic role for H19, an aberrant expression have been identified in a variety of cancers: breast, ovarian, hepatocellular, gastric, lung, colon, esophagus [ — ].
Significantly high levels of MALAT1 expression were detected in lung cancer, prostate cancer, colorectal cancer, hepatocellular carcinomas, gynecologic endometrial, cervical cancer, osteosarcoma [ — ].
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There are identified lncRNAs that appear to have tumor suppressor function in carcinogenesis. For GAS5 growth arrest specific 5 lncRNA, it was found to play an important role in apoptosis induction; studies have reported a significantly reduced GAS5 levels of expression in breast cancer and prostate cancer [ , ]. Another report shows that GAS5 low level of expression is associated with poor prognosis in hepatocellular carcinoma [ ].
MEG3 maternally expressed 3 is lncRNAs that presents a reduced expression in several types of cancer. Several experimental evidences demonstrate that MEG3 interacts with p53 tumor suppressor gene and regulates p53 target gene expression, therefore, inhibits tumor cell proliferation and cancer progression. Aberrant levels of MEG3 expression have been identified in glioblastoma, ovarian, colon, cervical, lung cancer [ — ]. In literature, there are a relatively small number of experimental data showing an association regarding lncRNAs involvement in cervical carcinogenesis, but due to high interest shown toward these molecules the number is growing fast.
List of lncRNAs expressed in cervical cancer [ — ]. Methylation status of integrated HPV depends of viral life cycle as well as of neoplastic transformation, this making HPV methylome a potential tool in cancer diagnostic. HPV genome methylation status depends on the viral life cycle and is associated with neoplastic progression.
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Methylation of the viral genome may be a part of a mechanism involved in innate response to pathogens by which the host attempts to suppress viral gene expression. The authors note that in HeLa cells, HPV18 genome chromatin histone modification status correlates with the occupancy of host transcriptional machinery specifically within the LCR [ ]. Mirabello et al. Evaluation of cervical samples from HPV positive women, presenting precancerous lesions or invasive ones, showing that the hypomethylation degree in LCR and E6 gene region increase with the increasing of lesion severity.
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These data convinced the authors to conclude that neoplastic transformation could be suppressed by hypermethylation, while hypomethylation accompanies or leads to progression toward cancer [ ]. A decrease in methylation in the transcriptional enhancer region within the LCR was observed in terminally differentiated epithelial compartment and meanwhile an increase in methylation within the region of the LCR containing the early promoter was noted [ ].
Another study highlighted heterogeneity of methylation status among patients, even in samples from the same patient. In most of the HPV genome sites, hypermethylation is associated better with carcinoma than with dysplastic lesions [ ]. The clinical samples showed partial or total methylation in HPV enhancer region, while in asymptomatic patient's, samples were fully unmethylated.
Viral promoter was reported to be methylated in tumor samples and in cervical smears [ ]. These studies indicate that methylation status of viral oncogenes in cervical lesions could be the result of transcriptional activity level and not an event that leads toward neoplastic progression.
Further studies regarding the influence of DNA methylation on viral life cycle focused on E2 early gene involved in viral transcription and replication gene methylation. The conclusion was that methylation status of E2BS may vary during the viral life cycle, this giving an insight on E2 modulation function during progression of infection [ ]. E2BS is more frequently found in a hypermethylated state in cervical lesions with extrachromosomal state of viral genome, while upon integration in the host genome, it was found to be hypomethylated, except the cases in which viral genome integrates as a concatemer, when only a small proportion are found hypomethylated and most of them hypermethylated [ ].
All this experimentally observations conclude that HPV genome methylation status could hold a prognostic and progression value for cervical lesions. Cancer epigenome is currently in the researchers spotlight due to the fact that all the epigenetic changes that accompany cervical carcinogenesis can be exploited as biomarkers. Thus, once deciphered, the epigenetic peculiarities of cervical cancer might be used in the development of new alternatives for screening or for the assessment of prognostic [ ].
On the other hand, the reversible nature of epigenetic alterations makes them attractive targets for new therapeutic approaches. Some of these discoveries have been proposed as investigation methods or resulted in new treatment approaches and commercial tests [ ]. By far, the most studied epigenetic changes are the methylation patterns, especially the methylation markers of the host. Abnormal methylation of promoters of tumor suppressor genes is common in different type of cancers with the prospect of becoming a biomarker in oncology [ ].
As the methylation profile of these genes increases with the severity of cervical lesions, their status might be used as potential biomarker for early detection of cervical cancer disease [ ]. For a better stratification of cervical cancer and precursor lesions, different specific methylation panels have been suggested [ ]. Siegel et al. The studies that associate the methylation profile with cervical lesion severity have resulted in a commercial test GynTect [ ].
So, this methylation assays might be use as a secondary marker after HPV DNA testing in order to guide the subsequent clinical approach referral to colposcopy or initiating a certain therapy [ ]. Other authors correlated changes in host DNA methylation with the development of drug resistance.
Chen et al. The methylation of Casp8AP2 gene resulted in increased drug resistance in different cells. Masuda et al. Iida et al. Regarding the methylation of viral DNA, data are still under debate. While some authors have suggested that it is a defense mechanism of the host cell, others considered it is a way by which the virus contributes to persistent infection. Other researchers considered that neoplastic transformation may be suppressed by HPV CpG methylation, while demethylation occurs as the cause of or concomitant with neoplastic progression [ ].
Also, Mirabello et al.
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Moreover, Wentzensen et al. Cervical carcinogenesis is accompanied also by altered expression of methyltransferases. For therapeutic purpose, Hamamoto et al.
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This gene encodes a HMT that methylate the H3K9 lysine residue and its hyperexpression correlates with carcinogenesis. These results showed that infection with different HPV genotypes differently interfere with epigenetic mechanisms. Molecular investigations of cervical tumors and cell lines immortalized with HPV have shown that, from all ncRNA molecules, miRNAs profile is significantly changed when compared to normal tissue, even in early stages of carcinogenesis [ ]. Zheng et al. Li et al. In Chinese population, Zhou et al. Epigenetic changes through methylation of miRNAs might correlate with cervical disease.
On animal model, Liu et al. Also, miRNAs might modulate the sensitivity to chemotherapy. Therefore, miRNA deregulation may become a target of the investigations for evaluating the effectiveness of treatments in cervical cancer [ ]. All these data underline the importance of epigenetic modification in tumor development and cervical cancer risk assessment. Epigenetic alterations could be used as biomarkers for the prognosis and evolution of the disease and for therapy response prediction.
New techniques in epigenetic investigations may yield better detection systems in order to identify new and sensitive biomarkers that might contribute to improved screening assays, new therapeutic approaches, and prediction biomarkers.