Suppr超能文献

口腔白斑和口腔鳞状细胞癌中肿瘤抑制基因的启动子高甲基化谱

Promoter hypermethylation profile of tumour suppressor genes in oral leukoplakia and oral squamous cell carcinoma.

作者信息

Asokan G S, Jeelani S, Gnanasundaram N

机构信息

Associate Professor, Department of Oral Medicine and Radiology, Tagore Dental College and Hospital , Chennai, India .

Reader, Department of Oral Medicine and Radiology, Indira Gandhi Institute of Dental Science , Pondicherry, India .

出版信息

J Clin Diagn Res. 2014 Oct;8(10):ZC09-12. doi: 10.7860/JCDR/2014/9251.4949. Epub 2014 Oct 20.

Abstract

PURPOSE OF THE STUDY

The present study was conducted to evaluate epigenetic alteration of five tumour suppressor genes in the oral precancer and cancer patients.

MATERIALS AND METHODS

The study was carried out in three groups namely control group of five people (normal healthy individuals), 10 oral leukoplakia patients and 10 oral squamous cell carcinoma patients. Incisional biopsy was done and part of the tissue sent for histological examination and part of tissue sent for hypermethylation study of p16, p15, hMLH, MGMT, E-cadherin tumour suppressor genes. Methylation specific polymerase chain reaction was carried out for detecting methylation in promoter regions of tumour suppressor genes. The resultant PCR products were run in a 2.5% agarose gel and the promoter hypermethylation status of the five tumour suppressor genes were analysed.

RESULTS

In oral Leukoplakia patients, 60% of methylation in the case of p16 gene, 30% of methylation in the case of MGMT gene and 60% of methylation in the case of E-cadherin gene. In oral Squamous cell carcinoma patients, 60% of methylation in the case of p16 gene, 40% of methylation in the case of MGMT, 60% of methylation in the case of E-cadherin gene, 20% in case of p15,10% in case of hMLH gene.

CONCLUSION

Our results suggest that epigenetic mechanisms of inactivation of tumour suppressor genes, such as aberrant methylation of p16 and E-cadherin genes occur early in head and neck tumourigenesis and might play a role in the progression of these lesions.

摘要

研究目的

本研究旨在评估口腔癌前病变和癌症患者中五个肿瘤抑制基因的表观遗传改变。

材料与方法

本研究分为三组,即五名正常健康个体组成的对照组、10名口腔白斑患者和10名口腔鳞状细胞癌患者。进行了切取活检,一部分组织送去做组织学检查,另一部分组织送去做p16、p15、hMLH、MGMT、E-钙黏蛋白肿瘤抑制基因的高甲基化研究。采用甲基化特异性聚合酶链反应检测肿瘤抑制基因启动子区域的甲基化情况。将所得的PCR产物在2.5%的琼脂糖凝胶中进行电泳,并分析五个肿瘤抑制基因的启动子高甲基化状态。

结果

在口腔白斑患者中,p16基因甲基化率为60%,MGMT基因甲基化率为30%,E-钙黏蛋白基因甲基化率为60%。在口腔鳞状细胞癌患者中,p16基因甲基化率为60%,MGMT基因甲基化率为40%,E-钙黏蛋白基因甲基化率为60%,p15基因甲基化率为20%,hMLH基因甲基化率为10%。

结论

我们的结果表明,肿瘤抑制基因失活的表观遗传机制,如p16和E-钙黏蛋白基因的异常甲基化,在头颈部肿瘤发生早期就会出现,并可能在这些病变的进展中发挥作用。

相似文献

1
Promoter hypermethylation profile of tumour suppressor genes in oral leukoplakia and oral squamous cell carcinoma.
J Clin Diagn Res. 2014 Oct;8(10):ZC09-12. doi: 10.7860/JCDR/2014/9251.4949. Epub 2014 Oct 20.
4
Aberrant promoter hypermethylation of p16 and MGMT genes in oral squamous cell carcinomas and the surrounding normal mucosa.
J Cancer Res Clin Oncol. 2006 Nov;132(11):735-43. doi: 10.1007/s00432-006-0122-8. Epub 2006 Jun 22.
5
Aberrant promoter hypermethylation of multiple genes in head and neck squamous cell carcinoma.
Am J Otolaryngol. 2005 Jan-Feb;26(1):12-7. doi: 10.1016/j.amjoto.2004.06.007.
8
Epigenetic abnormalities in cutaneous squamous cell carcinomas: frequent inactivation of the RB1/p16 and p53 pathways.
Br J Dermatol. 2006 Nov;155(5):999-1005. doi: 10.1111/j.1365-2133.2006.07487.x.
9
Promoter hypermethylation of multiple genes in early gastric adenocarcinoma and precancerous lesions.
Hum Pathol. 2009 Nov;40(11):1534-42. doi: 10.1016/j.humpath.2009.01.029. Epub 2009 Aug 19.
10
High frequency of hypermethylation of p14, p15 and p16 in oral pre-cancerous lesions associated with betel-quid chewing in Sri Lanka.
J Oral Pathol Med. 2008 Sep;37(8):475-9. doi: 10.1111/j.1600-0714.2008.00644.x. Epub 2008 Feb 17.

引用本文的文献

2
SP1 Gene Methylation in Head and Neck Squamous Cell Cancer in HPV-Negative Patients.
Genes (Basel). 2024 Feb 23;15(3):281. doi: 10.3390/genes15030281.
4
Genome-wide DNA methylation profiling of HPV-negative leukoplakia and gingivobuccal complex cancers.
Clin Epigenetics. 2023 May 27;15(1):93. doi: 10.1186/s13148-023-01510-z.
5
An Overview of DNA Methylation Indicators for the Course of Oral Precancer.
Appl Bionics Biomech. 2022 Aug 26;2022:6468773. doi: 10.1155/2022/6468773. eCollection 2022.
8
Saliva Gene Promoter Hypermethylation as a Biomarker in Oral Cancer.
J Clin Med. 2021 Apr 29;10(9):1931. doi: 10.3390/jcm10091931.

本文引用的文献

1
Methylation as a biomarker for head and neck cancer.
Oral Oncol. 2014 Jun;50(6):587-92. doi: 10.1016/j.oraloncology.2014.02.015. Epub 2014 Mar 20.
2
Epigenetic mechanisms in oral carcinogenesis.
Future Oncol. 2012 Nov;8(11):1407-25. doi: 10.2217/fon.12.138.
3
Environmental chemical exposures and human epigenetics.
Int J Epidemiol. 2012 Feb;41(1):79-105. doi: 10.1093/ije/dyr154. Epub 2011 Dec 13.
4
CpG island methylation status of miRNAs in esophageal squamous cell carcinoma.
Int J Cancer. 2012 Apr 1;130(7):1607-13. doi: 10.1002/ijc.26171. Epub 2011 Aug 24.
7
High frequency of hypermethylation of p14, p15 and p16 in oral pre-cancerous lesions associated with betel-quid chewing in Sri Lanka.
J Oral Pathol Med. 2008 Sep;37(8):475-9. doi: 10.1111/j.1600-0714.2008.00644.x. Epub 2008 Feb 17.
8
Methylation profile of genes CDKN2A (p14 and p16), DAPK1, CDH1, and ADAM23 in head and neck cancer.
Cancer Genet Cytogenet. 2007 Feb;173(1):31-7. doi: 10.1016/j.cancergencyto.2006.09.008.
9
Ros-induced histone modifications and their role in cell survival and cell death.
Drug Metab Rev. 2006;38(4):755-67. doi: 10.1080/03602530600959649.
10
Aberrant promoter hypermethylation of p16 and MGMT genes in oral squamous cell carcinomas and the surrounding normal mucosa.
J Cancer Res Clin Oncol. 2006 Nov;132(11):735-43. doi: 10.1007/s00432-006-0122-8. Epub 2006 Jun 22.

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验