scholarly journals DNA Methylation Profiling of MYC, SMAD2/3 and DNMT3A in Colorectal Cancer

2021 ◽  
Author(s):  
Seyedeh Elham Norollahi ◽  
Maryam Gholamniya Foumani ◽  
Maryam Khoshbakht Pishkhan ◽  
Afshin Shafaghi ◽  
Majid Alipour ◽  
...  

Epigenetic modifications particularly DNA methylation is a common place and remarkable factor in carcinogenesis transformation. Conspicuously, previous findings have presented a cluster of irregular promoter methylation alterationsrelated with silencing of TSG (tumor suppressor genes), little is accepted regarding their sequential DNA methylation (Hypo and Hyper) modifications during the cancer progression. In this way, fluctuations of DNA methylation of many certain genes especially MYC, SMAD2/3 and DNMT3A have an impressive central key role in many different cancers like colorectal (CRC)one. CRC is distinguished by DNA methylation, which is related with tumorigenesis and also genomic instability. Importantly, molecular heterogeneity between multiple adenomas in different patients with CRC may show diverse developmental phenotypes for these kinds of tumors. Conclusively, studying of factors which are involved in CRC carcinogenesis, especially the alterations in epigenetic elements, such as DNA methylation besides the RNA remodeling, histone modification, histone acetylation and histone phosphorylation can be influential in order to find new therapeutic and diagnostic biomarkers in this type of malignancy. In this account, we tried to discuss and address the potential significant methylated modifications of these genes and their importance during the development of CRC carcinogenesis.

2018 ◽  
Vol 20 (suppl_6) ◽  
pp. vi109-vi109
Author(s):  
Wei Meng ◽  
Erica Hlavin Bell ◽  
Rajbir Singh ◽  
Joseph McElroy ◽  
Ilinca Popp ◽  
...  

2019 ◽  
Vol 110 (2) ◽  
pp. 828-832 ◽  
Author(s):  
Taishi Nakamura ◽  
Kohei Fukuoka ◽  
Yoshiko Nakano ◽  
Kai Yamasaki ◽  
Yuko Matsushita ◽  
...  

Thyroid ◽  
2020 ◽  
Vol 30 (2) ◽  
pp. 192-203
Author(s):  
Jong-Lyul Park ◽  
Sora Jeon ◽  
Eun-Hye Seo ◽  
Dong Hyuck Bae ◽  
Young Mun Jeong ◽  
...  

BMC Medicine ◽  
2014 ◽  
Vol 12 (1) ◽  
Author(s):  
Brittany N Lasseigne ◽  
Todd C Burwell ◽  
Mohini A Patil ◽  
Devin M Absher ◽  
James D Brooks ◽  
...  

PLoS ONE ◽  
2009 ◽  
Vol 4 (12) ◽  
pp. e8357 ◽  
Author(s):  
Toshinori Hinoue ◽  
Daniel J. Weisenberger ◽  
Fei Pan ◽  
Mihaela Campan ◽  
Myungjin Kim ◽  
...  

2019 ◽  
Vol 32 (6) ◽  
pp. 855-865 ◽  
Author(s):  
Philipp Jurmeister ◽  
Anne Schöler ◽  
Alexander Arnold ◽  
Frederick Klauschen ◽  
Dido Lenze ◽  
...  

2020 ◽  
pp. 1-10
Author(s):  
Louise Stögbauer ◽  
Christian Thomas ◽  
Andrea Wagner ◽  
Nils Warneke ◽  
Eva Christine Bunk ◽  
...  

OBJECTIVEChemotherapeutic options for meningiomas refractory to surgery or irradiation are largely unknown. Human telomerase reverse transcriptase (hTERT) promoter methylation with subsequent TERT expression and telomerase activity, key features in oncogenesis, are found in most high-grade meningiomas. Therefore, the authors investigated the impact of the demethylating agent decitabine (5-aza-2ʹ-deoxycytidine) on survival and DNA methylation in meningioma cells.METHODShTERT promoter methylation, telomerase activity, TERT expression, and cell viability and proliferation were investigated prior to and after incubation with decitabine in two benign (HBL-52 and Ben-Men 1) and one malignant (IOMM-Lee) meningioma cell line. The global effects of decitabine on DNA methylation were additionally explored with DNA methylation profiling.RESULTSHigh levels of TERT expression, telomerase activity, and hTERT promoter methylation were found in IOMM-Lee and Ben-Men 1 but not in HBL-52 cells. Decitabine induced a dose-dependent significant decrease of proliferation and viability after incubation with doses from 1 to 10 μM in IOMM-Lee but not in HBL-52 or Ben-Men 1 cells. However, effects in IOMM-Lee cells were not related to TERT expression, telomerase activity, or hTERT promoter methylation. Genome-wide methylation analyses revealed distinct demethylation of 14 DNA regions after drug administration in the decitabine-sensitive IOMM-Lee but not in the decitabine-resistant HBL-52 cells. Differentially methylated regions covered promoter regions of 11 genes, including several oncogenes and tumor suppressor genes that to the authors’ knowledge have not yet been described in meningiomas.CONCLUSIONSDecitabine decreases proliferation and viability in high-grade but not in benign meningioma cell lines. The effects of decitabine are TERT independent but related to DNA methylation changes of promoters of distinct tumor suppressor genes and oncogenes.


Sign in / Sign up

Export Citation Format

Share Document