Epigenetic Mechanisms in Head and Neck Cancer

Osorio, Julio; Castillo, Andrés

doi:10.5772/61135

Cited by 4 publications

(9 citation statements)

References 125 publications

(158 reference statements)

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“…Approximately 50% of genes contain CGIs DNMTs add a methyl group (CH 3 ) to the carbon in the 5 position of cytosine, converting it to 5-methylcytosine. The donor of the methyl group is S-adenosylmethionine (SAM), which is converted to S-adenosylhomocysteine (SAH) (updated from Luczak and Jagodziński 2006;Osorio and Castillo 2016) in their promoter regions (Luczak and Jagodziński 2006;Magić et al 2013; Reyngold and Chan 2018) and methylation mostly occurs in the promoter region or the first exon sequence (Luczak and Jagodziński 2006;Gopisetty et al 2006;Arantes et al 2014). Methylation is catalyzed by members of the family of DNA methyltransferases (DNMTs) composed of DNMT1, DNMT2, DNMT3A, and DNMT3B.…”

Section: Methylation Of Dnamentioning

confidence: 99%

“…DNMT1 is a maintenance enzyme responsible for methylation during replication, while de novo methylation is catalyzed by DNMT3A and DNMT3B (Luczak and Jagodziński 2006;Arantes et al 2014). The DNMT family enzymes use S-adenosylmethionine (SAM) as a methyl donor, which is converted to S-adenosylhomocysteine (SAH) (Luczak and Jagodziński 2006;Osorio and Castillo 2016).…”

Section: Methylation Of Dnamentioning

confidence: 99%

“…miRNAs MicroRNAs (miRNAs), one of the classes of small non-coding RNA, are short (17-25 nucleotides) single-stranded RNAs that are partially complementary to the 3′-untranslated region of messenger RNAs. Through binding to mRNAs they cause their degradation or inhibit their translation, and as a result they modulate expression of nearly 30% of human genes (Lee and Dutta 2009;Shiiba et al 2010;Osorio and Castillo 2016). miRNAs participate in many cellular processes like proliferation, differentiation, development, and apoptosis (Bartel 2004;Kimura et al 2010;Osorio and Castillo 2016).…”

Section: Non-coding Rnasmentioning

confidence: 99%

“…Through binding to mRNAs they cause their degradation or inhibit their translation, and as a result they modulate expression of nearly 30% of human genes (Lee and Dutta 2009;Shiiba et al 2010;Osorio and Castillo 2016). miRNAs participate in many cellular processes like proliferation, differentiation, development, and apoptosis (Bartel 2004;Kimura et al 2010;Osorio and Castillo 2016). Furthermore, miRNAs may be classified as oncogenes or suppressor genes based on their cancer-related expression.…”

Section: Non-coding Rnasmentioning

confidence: 99%

“…An epigenetic pattern may be modulated by external factors such as diet, alcohol, tobacco, toxins, or pharmaceutical treatment (Ghantous et al 2018). Epigenetic mechanisms are associated with carcinogenesis of numerous cancers (Park et al 2011;Osorio and Castillo 2016) and play an important role in the development of head and neck squamous cell carcinoma (HNSCC).…”

Section: Introductionmentioning

confidence: 99%

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Epigenetic Modifications in Head and Neck Cancer

et al. 2019

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Head and neck squamous cell carcinoma (HNSCC) is the sixth most common human malignancy in the world, with high mortality and poor prognosis for patients. Among the risk factors are tobacco and alcohol intake, human papilloma virus, and also genetic and epigenetic modifications. Many studies show that epigenetic events play an important role in HNSCC development and progression, including DNA methylation, chromatin remodeling, histone posttranslational covalent modifications, and effects of non-coding RNA. Epigenetic modifications may influence silencing of tumor suppressor genes by promoter hypermethylation, regulate transcription by microRNAs and changes in chromatin structure, or induce genome instability through hypomethylation. Moreover, getting to better understand aberrant patterns of methylation may provide biomarkers for early detection and diagnosis, while knowledge about target genes of microRNAs may improve the therapy of HNSCC and extend overall survival. The aim of this review is to present recent studies which demonstrate the role of epigenetic regulation in the development of HNSCC.

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Section: Methylation Of Dnamentioning

confidence: 99%

Section: Methylation Of Dnamentioning

confidence: 99%

Section: Non-coding Rnasmentioning

confidence: 99%

Section: Non-coding Rnasmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Epigenetic Modifications in Head and Neck Cancer

et al. 2019

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Towards system genetics analysis of head and neck squamous cell carcinoma using the mouse model, cellular platform, and clinical human data

Zohud,

Lone,

Nashef

et al. 2023

Anim Models and Exp Med

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Head and neck squamous cell cancer (HNSCC) is a leading global malignancy. Every year, More than 830 000 people are diagnosed with HNSCC globally, with more than 430 000 fatalities. HNSCC is a deadly diverse malignancy with many tumor locations and biological characteristics. It originates from the squamous epithelium of the oral cavity, oropharynx, nasopharynx, larynx, and hypopharynx. The most frequently impacted regions are the tongue and larynx. Previous investigations have demonstrated the critical role of host genetic susceptibility in the progression of HNSCC. Despite the advances in our knowledge, the improved survival rate of HNSCC patients over the last 40 years has been limited. Failure to identify the molecular origins of development of HNSCC and the genetic basis of the disease and its biological heterogeneity impedes the development of new therapeutic methods. These results indicate a need to identify more genetic factors underlying this complex disease, which can be better used in early detection and prevention strategies. The lack of reliable animal models to investigate the underlying molecular processes is one of the most significant barriers to understanding HNSCC tumors. In this report, we explore and discuss potential research prospects utilizing the Collaborative Cross mouse model and crossing it to mice carrying single or double knockout genes (e.g. Smad4 and P53 genes) to identify genetic factors affecting the development of this complex disease using genome‐wide association studies, epigenetics, microRNA, long noncoding RNA, lncRNA, histone modifications, methylation, phosphorylation, and proteomics.

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Molecular Genetics of Peutz-Jegher Syndrome

Monica¹,

Auerkari²

2018

Proceedings of the 11th International Dentistry Scientific Meeting (IDSM 2017)

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Peutz-Jeghers Syndrome (PJS) is one of the inherited syndromes associated with polyposis. It is characterized by mucocutaneous pigmentation, especially in the vermilion border of the lips and gastrointestinal tract. This is known as hamartomatous polyposis. The disease results from an autosomal dominant mutation localized in the LKB1 (liver kinase B1) or STK11 (serine/threonine kinase 11) gene on chromosome 19p13.3. The STK11 gene plays a role as a tumor suppressor gene. Mutation in STK11 results in an abnormally shortened or truncated protein, transcriptional splicing errors, and loss of kinase activity. Therefore, somatic inactivation of STK11 will cause formation of hamartomas and tumors in PJS. Yoon et al. identified several types of STK11 gene mutation, including nonsense, missense, splicing site, and ameshift mutations. The other mutation STK11 lead to complications such as cancers, surgical treatment, and increased numbers of polyps. Another mechanism for the inactivation of tumor suppresor genes is promoter hypermethylation of normally unmethylated CpG islands located in promoter regions of DNA repair and tumor suppressor genes. In conclusion, STK11/LKB1 gene mutation is the etiology of PJS.

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Epigenetic Mechanisms in Head and Neck Cancer

Cited by 4 publications

References 125 publications

Epigenetic Modifications in Head and Neck Cancer

Epigenetic Modifications in Head and Neck Cancer

Towards system genetics analysis of head and neck squamous cell carcinoma using the mouse model, cellular platform, and clinical human data

Molecular Genetics of Peutz-Jegher Syndrome

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