Promoter Methylation of Tumor Suppressors in Thyroid Carcinoma: A Systematic Review

被引:0
作者
Sheikholeslami, Sara [1 ]
Zarif-Yeganeh, Marjan [1 ]
Farashi, Samaneh [2 ,3 ]
Azizi, Fereidoun [4 ]
Kia, Sima Kheradmand [5 ]
Teimoori-Toolabi, Ladan [6 ]
Hedayati, Mehdi [1 ]
机构
[1] Shahid Beheshti Univ Med Sci, Cellular & Mol Endocrine Res Ctr, Res Inst Endocrine Res Ctr, Tehran, Iran
[2] Queensland Univ Technol, Australian Prostate Canc Res Ctr Queensland, Sch Biomed Sci, Canc Program,Inst Hlth & Biomed Innovat, Brisbane, Qld 4102, Australia
[3] Translat Res Inst, Woolloongabba, Qld 4102, Australia
[4] Shahid Beheshti Univ Med Sci, Endocrine Res Ctr, Res Inst Endocrine Sci, Tehran, Iran
[5] Sanquin, Lab Red Blood Cell Diagnost, Amsterdam, Netherlands
[6] Pasteur Inst Iran, Biotechnol Res Ctr, Mol Med Dept, Tehran, Iran
关键词
DNA methylation; Tumor suppressor gene; Epigenetic; Thyroid cancer; Neoplasm; BRAF MUTATION; TISSUE INHIBITOR; GENE; CANCER; RASSF1A; PATHWAY; SLC5A8; HYPERMETHYLATION; EXPRESSION; KINASE;
D O I
暂无
中图分类号
R1 [预防医学、卫生学];
学科分类号
1004 ; 120402 ;
摘要
Background: The tumor suppressor genes play a critical role in cellular and molecular mechanisms such as cell cycle processes, cell differentiation and apoptosis. Aberrant DNA methylation of tumor suppressor genes and subsequent gene expression changes have shown to be involved in the initiation and progression of various malignancies including thyroid malignancies. In this review, we investigated what is known about the impact of promoter hypermethylation on the key tumor suppressor genes known to be involved in cell growth and/or apoptosis of thyroid cancer. Methods: The most important databases were searched for research articles until June 2020 to identify reported tumor suppressor genes that are modulated by methylation modulation changes in thyroid carcinoma. Following the inclusion and exclusion criteria, 26 studies were reviewed using the full text to meet the inclusion and exclusion criteria. Results: The tumor suppressor genes reviewed here are suggestive biomarkers and potential targetable drugs. Inactivation of RASSF1A, DAPK1, SLCFA8, and TSHR through aberrant epigenetic methylation could activate BRAF/MEK/ERK kinase pathways with potential clinical implications in thyroid cancer patients. RAR beta 2 and RUNX3 could suppress cell cycle and induce apoptosis in malignant cells. TIMP3 and PTEN could prevent angiogenesis and invasion through PIP3 pathway and arrest VEFG activity. Conclusion: The methylation status of key genes in various types of thyroid malignancies could be used in early diagnosis as well as differentiation of malignant and benign thyroid. This is valuable in drug repurposing and discovering alternative treatments or preventions in thyroid cancer.
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页码:2461 / 2472
页数:12
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