GPER is inactivated by promoter methylation and potentially functions as a tumor suppressor in breast cancer

2014 ◽  
Vol 74 (S 01) ◽  
Author(s):  
C Weißenborn ◽  
T Ignatov ◽  
SD Costa ◽  
AC Zenclussen ◽  
A Ignatov
Keyword(s):  
Breast Cancer ◽  
Tumor Suppressor ◽  
Promoter Methylation

scholarly journals Promoter Methylation Status Modulate the Expression of Tumor Suppressor (RbL2/p130) Gene in Breast Cancer

PLoS ONE ◽  
2015 ◽  
Vol 10 (8) ◽  
pp. e0134687 ◽  
Author(s):  
Farman Ullah ◽  
Taimoor Khan ◽  
Nawab Ali ◽  
Faraz Arshad Malik ◽  
Mahmood Akhtar Kayani ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Tumor Suppressor ◽  
Promoter Methylation ◽  
Methylation Status ◽  
Promoter Methylation Status

scholarly journals Detection of promoter methylation of tumor suppressor genes in serum DNA of breast cancer cases and benign breast disease controls

Epigenetics ◽  
2012 ◽  
Vol 7 (11) ◽  
pp. 1258-1267 ◽  
Author(s):  
Susan R. Sturgeon ◽  
Raji Balasubramanian ◽  
Catherine Schairer ◽  
Hyman B. Muss ◽  
Regina G. Ziegler ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Tumor Suppressor ◽  
Promoter Methylation ◽  
Tumor Suppressor Genes ◽  
Benign Breast Disease ◽  
Breast Disease ◽  
Suppressor Genes ◽  
Serum Dna

scholarly journals DNA Methylation of Tumor Suppressor and Metastasis Suppressor Genes in Circulating Tumor Cells

2011 ◽  
Vol 57 (8) ◽  
pp. 1169-1177 ◽  
Author(s):  
Maria Chimonidou ◽  
Areti Strati ◽  
Alexandra Tzitzira ◽  
Georgia Sotiropoulou ◽  
Nikos Malamos ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Dna Methylation ◽  
Tumor Suppressor ◽  
Tumor Cells ◽  
Promoter Methylation ◽  
Operable Breast Cancer ◽  
Metastasis Suppressor ◽  
Healthy Individuals ◽  
Suppressor Genes ◽  
Metastasis Suppressor Genes

BACKGROUND Circulating tumor cells (CTCs) are associated with prognosis in a variety of human cancers and have been proposed as a liquid biopsy for follow-up examinations. We show that tumor suppressor and metastasis suppressor genes are epigenetically silenced in CTCs isolated from peripheral blood of breast cancer patients. METHODS We obtained peripheral blood from 56 patients with operable breast cancer, 27 patients with verified metastasis, and 23 healthy individuals. We tested DNA extracted from the EpCAM-positive immunomagnetically selected CTC fraction for the presence of methylated and unmethylated CST6, BRMS1, and SOX17 promoter sequences by methylation-specific PCR (MSP). All samples were checked for KRT19 (keratin 19, formerly CK-19) expression by reverse-transcription quantitative PCR. RESULTS In CTCs of patients with operable breast cancer, promoter methylation of CST6 was observed in 17.9%, BRMS1 in 32.1%, and SOX17 in 53.6% of patients. In CTCs of patients with verified metastasis, promoter methylation of CST6 was observed in 37.0%, BRMS1 in 44.4%, and SOX17 in 74.1%. In healthy individuals, promoter methylation of CST6 was observed in 4.3%, BRMS1 in 8.7%, and SOX17 in 4.3%. DNA methylation of these genes for both operable and metastatic breast cancer was significantly different from that of the control population. CONCLUSIONS DNA methylation of tumor suppressor and metastasis suppressor genes is a hallmark of CTCs and confirms their heterogeneity. Our findings add a new dimension to the molecular characterization of CTCs and may underlie the acquisition of malignant properties, including their stem-like phenotype.

Efficacy of decitabine in malignant meningioma cells: relation to promoter demethylation of distinct tumor suppressor and oncogenes and independence from TERT

2020 ◽  
pp. 1-10
Author(s):  
Louise Stögbauer ◽  
Christian Thomas ◽  
Andrea Wagner ◽  
Nils Warneke ◽  
Eva Christine Bunk ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Tumor Suppressor ◽  
Promoter Methylation ◽  
Tumor Suppressor Genes ◽  
Telomerase Activity ◽  
High Grade ◽  
Htert Promoter ◽  
Men 1 ◽  
Meningioma Cell ◽  
Tert Expression

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.

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