Journal of Prevention and Treatment for Stomatological Diseases ›› 2020, Vol. 28 ›› Issue (10): 613-622.doi: 10.12016/j.issn.2096-1456.2020.10.001

• Expert Forum • Previous Articles     Next Articles

Epigenetic and oral squamous cell carcinoma

WANG Anxun()   

  1. Department of Oral and Maxillofacial Surgery, the First Affiliated Hospital of Sun Yat-sen University, Guangzhou 510080, China
  • Received:2020-01-20 Revised:2020-03-04 Online:2020-10-20 Published:2020-09-01
  • Contact: Anxun WANG E-mail:wang_anxun@aliyun.com

Abstract:

In recent decades, although great progress has been made on the diagnosis and treatment of oral squamous cell carcinoma (OSCC), its 5-year survival rate has not been significantly improved. The basic reason is the unclear pathogenesis, lack of effective molecular markers for assessing invasion, metastasis, and recurrence as well as therapeutic targets. The present view is that genetic and epigenetic abnormalities are related to the occurrence and development of OSCC. Epigenetic inheritance is a biological behavior that can be regulated and reversed, and it plays an important role in the occurrence and development of malignant tumors. First, this review will describe the role of epigenetic modifications in the development of OSCC in combination with our research and the latest research progress of epigenetics, including DNA methylation, RNA methylation, short noncoding RNAs (miRNAs, etc.), long noncoding RNAs, circular RNAs, histone modifications (acetylation and methylation), chromatin remodeling and genomic imprinting. Then, we will analyze the value of epigenetic studies in the prevention, diagnosis, and targeted therapy of OSCC.

Key words: epigenetic, oral squamous cell carcinoma, DNA methylation, RNA methylation, non-coding RNA, histone modification, biomarker, prevention, diagnosis, target therapy

CLC Number: 

  • R78

Figure 1

Mechanism of miRNAs regulating the proliferation, invasion, metastasis and drug resistance of OSCC miR: mirco-RNA; OSCC: oral squamous cell carcinoma; ABCG2: ATP-binding cassette superfamily G2 gene; SOD2: superoxide dismutase 2; MAPK1: mitogen-activated protein kinase 1; Vim: vimentin; E-cad: E-Cadherin; Snai2: snail family zinc finger 2; EMT: epithelial-mesenchymal transition; CSC: cancer stem cell; Bmi1: B-cell-specific Moloney murine leukemia virus insertion site 1; ROCK1: Rho-associated oiled-coil containing protein kinase 1; RhoA: Ras homolog gene family, member A; EZH2: enhancer of Zeste homolog 2; ZEB2: Zinc finger E-box-binding homeobox 2; Twist1: Twist family bHLH transcription factor 1; MAP2K1: mitogen-activated protein kinase 1 interacting protein 1; IGF1R: insulin-like growth factor 1 receptor; mTOR: mammalian target of rapamycin; HPGD: 15-hydroxyprostaglandin dehydrogenase; DND1: Deadend 1; CDKN1B: cyclin-dependent kinase inhibitor 1B"

Figure 2

The genetics and epigenetics of OSCC OSCC: oral squamous cell carcinoma; ncRNA: non-coding RNA; sncRNA: small non-codingRNA"

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