scholarly journals Promoter aberrant methylation status of ADRA1A is associated with hepatocellular carcinoma

Epigenetics ◽  
2020 ◽  
Vol 15 (6-7) ◽  
pp. 684-701
Author(s):  
Guoqiao Chen ◽  
Xiaoxiao Fan ◽  
Yirun Li ◽  
Lifeng He ◽  
Shanjuan Wang ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Methylation Status ◽  
Aberrant Methylation

Aberrant methylation of tumour suppressor genes WT1, GATA5 and PAX5 in hepatocellular carcinoma

2016 ◽  
Vol 54 (12) ◽  
Author(s):  
Martin Mžik ◽  
Marcela Chmelařová ◽  
Stanislav John ◽  
Jan Laco ◽  
Ondřej Slabý ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Promoter Methylation ◽  
Mrna Level ◽  
Methylation Status ◽  
Tumour Suppressor ◽  
Tumour Suppressor Genes ◽  
Aberrant Methylation ◽  
Suppressor Genes ◽  
Tissue Samples ◽  
Differentially Methylated Genes

AbstractBackground:Aberrant hypermethylation of tumour suppressor genes (TSGs) occurring in hepatocellular carcinoma (HCC) could provide a mean of molecular characterisation of this cancer. The aim of this study was to investigate promoter methylation and gene expression of selected TSGs in HCC to identify candidate genes for further validation as potential biomarkers.Methods:Methylation-specific multiplex ligation-dependent probe amplification method was used to measure the methylation status of 25 TSGs in 49 HCC samples and 36 corresponding non-cancerous liver tissue samples. Relative expression of the differentially methylated genes was assessed at the mRNA level using quantitative PCR.Results:We observed a significantly higher methylation in genesConclusions:HCC evince aberrant promoter methylation of

scholarly journals Aberrant methylation status of SPG20 promoter in hepatocellular carcinoma: A potential tumor metastasis biomarker

2019 ◽  
Vol 233-234 ◽  
pp. 48-55
Author(s):  
Lifeng He ◽  
Xiaoxiao Fan ◽  
Yirun Li ◽  
Bin Cui ◽  
Zhaoqi Shi ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Tumor Metastasis ◽  
Methylation Status ◽  
Aberrant Methylation

scholarly journals A Genome-Wide Investigation of Effects of Aberrant DNA Methylation on the Usage of Alternative Promoters in Hepatocellular Carcinoma

2022 ◽  
Vol 11 ◽  
Author(s):  
Yuting Dong ◽  
Xiaozhao Liu ◽  
Bijun Jiang ◽  
Siting Wei ◽  
Bangde Xiang ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Dna Methylation ◽  
Negative Correlation ◽  
Promoter Activity ◽  
Methylation Status ◽  
Functional Enrichment ◽  
Diagnostic Model ◽  
Aberrant Methylation ◽  
Alternative Promoters ◽  
Rna Seq

BackgroundThe alternative usage of promoters provides a way to regulate gene expression, has a significant influence on the transcriptome, and contributes to the cellular transformation of cancer. However, the function of alternative promoters (APs) in hepatocellular carcinoma (HCC) has not been systematically studied yet. In addition, the potential mechanism of regulation to the usage of APs remains unclear. DNA methylation, one of the most aberrant epigenetic modifications in cancers, is known to regulate transcriptional activity. Whether DNA methylation regulates the usage of APs needs to be explored. Here, we aim to investigate the effects of DNA methylation on usage of APs in HCC.MethodsPromoter activities were calculated based on RNA-seq data. Functional enrichment analysis was implemented to conduct GO terms. Correlation tests were used to detect the correlation between promoter activity and methylation status. The LASSO regression model was used to generate a diagnostic model. Kaplan–Meier analysis was used to compare the overall survival between high and low methylation groups. RNA-seq and whole-genome bisulfite sequencing (WGBS) in HCC samples were performed to validate the correlation of promoter activity and methylation.ResultsWe identified 855 APs in total, which could be well used to distinguish cancer from normal samples. The correlation of promoter activity and DNA methylation in APs was observed, and the APs with negative correlation were defined as methylation-regulated APs (mrAPs). Six mrAPs were identified to generate a diagnostic model with good performance (AUC = 0.97). Notably, the majority of mrAPs had CpG sites that could be used to predict clinical outcomes by methylation status. Finally, we verified 85.6% of promoter activity variation and 92.3% of methylation changes in our paired RNA-seq and WGBS samples, respectively. The negative correlation between promoter activity and methylation status was further confirmed in our HCC samples.ConclusionThe aberrant methylation status plays a critical role in the precision usage of APs in HCC, which sheds light on the mechanism of cancer development and provides a new insight into cancer screening and treatment.

Aberrant STAT1 methylation as a non-invasive biomarker in blood of HCV induced hepatocellular carcinoma

2021 ◽  
pp. 1-9
Author(s):  
Umaira Zakir ◽  
Nadir Naveed Siddiqui ◽  
Faizan-ul-Hassan Naqvi ◽  
Rizma Khan
Keyword(s):  
Hepatocellular Carcinoma ◽  
Tumor Suppressor ◽  
Tumor Suppressor Genes ◽  
Methylation Status ◽  
Tumor Formation ◽  
Aberrant Methylation ◽  
Suppressor Genes ◽  
Non Invasive ◽  
Specific Pcr

BACKGROUND: Hepatocellular carcinoma (HCC) is one of the most common types of cancer in the world and a reason behind different oncogenes activation and tumor suppressor genes inactivation. Hyper-methylation of tumor suppressor genes including RASSF1a, GSTP1, p16, and APC cause gene silencing as well as tumor cell invasion. STAT 1 gene is a part of signaling cascade of JAK/STAT and any dysregulation in signaling has been implicated in tumor formation. OBJECTIVE: The current investigation focus on the methylation role of STAT1 gene as a non-invasive biomarker in the progression and diagnosis of hepatocellular carcinoma. METHODS: STAT1 gene methylation status in 46 HCV induced hepatocellular carcinoma patients and 40 non-HCC controls were examined by methylation specific PCR. STAT1 gene expression was examined by real time PCR and further validated by various bioinformatics tools. RESULTS: STAT1 methylation in HCV-induced HCC (67.4%) was significantly higher compared to the non-HCC controls (p< 0.01). However, mRNA expression of STAT1 gene in methylated groups was significantly lower compared to unmethylated groups (p< 0.05). Furthermore, insilco analysis of STAT1 validated our results and shown expression of STAT1 mRNA was lower in liver cancer with the median 24.3 (p= 0.085). CONCLUSION: After using peripheral blood samples we observed that STAT1 silencing caused by aberrant methylation could be used as potential non-invasive biomarker for the diagnosis of HCV induced hepatocellular carcinoma. We conclude that blood as a sample source could be used instead of biopsy for early detection of HCC.

Progressive alteration of DNA methylation of Alu, MGMT, MINT2, and TFPI2 genes in colonic mucosa during colorectal cancer development

2021 ◽  
pp. 1-6
Author(s):  
Ben Kang ◽  
Hyun Seok Lee ◽  
Seong Woo Jeon ◽  
Soo Yeun Park ◽  
Gyu Seog Choi ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Dna Methylation ◽  
Healthy Subjects ◽  
Large Scale ◽  
Methylation Status ◽  
Clinical Information ◽  
Field Cancerization ◽  
Aberrant Methylation ◽  
Clinical Value ◽  
Mortality And Morbidity

BACKGROUND: Colorectal cancer (CRC) is one of the leading causes of mortality and morbidity in the world. It is characterized by different pathways of carcinogenesis and is a heterogeneous disease with diverse molecular landscapes that reflect histopathological and clinical information. Changes in the DNA methylation status of colon epithelial cells have been identified as critical components in CRC development and appear to be emerging biomarkers for the early detection and prognosis of CRC. OBJECTIVE: To explore the underlying disease mechanisms and identify more effective biomarkers of CRC. METHODS: We compared the levels and frequencies of DNA methylation in 11 genes (Alu, APC, DAPK, MGMT, MLH1, MINT1, MINT2, MINT3, p16, RGS6, and TFPI2) in colorectal cancer and its precursor adenomatous polyp with normal tissue of healthy subjects using pyrosequencing and then evaluated the clinical value of these genes. RESULTS: Aberrant methylation of Alu, MGMT, MINT2, and TFPI2 genes was progressively accumulated during the normal-adenoma-carcinoma progression. Additionally, CGI methylation occurred either as an adenoma-associated event for APC, MLH1, MINT1, MINT31, p16, and RGS6 or a tumor-associated event for DAPK. Moreover, relatively high levels and frequencies of DAPK, MGMT, and TFPI2 methylation were detected in the peritumoral nonmalignant mucosa of cancer patients in a field-cancerization manner, as compared to normal mucosa from healthy subjects. CONCLUSION: This study identified several biomarkers associated with the initiation and progression of CRC. As novel findings, they may have important clinical implications for CRC diagnostic and prognostic applications. Further large-scale studies are needed to confirm these findings.

Aberrant Genes Promoter Methylation in Neural Crest-Derived Tumors

2012 ◽  
Vol 27 (4) ◽  
pp. 389-394 ◽  
Author(s):  
Annamaria La Torre ◽  
Lucia Anna Muscarella ◽  
Paola Parrella ◽  
Teresa Balsamo ◽  
Michele Bisceglia ◽  
...  
Keyword(s):  
Small Bowel ◽  
Neural Crest ◽  
Promoter Methylation ◽  
Methylation Status ◽  
Cpg Islands ◽  
Aberrant Methylation ◽  
Tumor Type ◽  
Epigenetic Landscape ◽  
Molecular Biomarker

Disturbances in the epigenetic landscape by aberrant methylation of CpG islands can lead to inactivation of cancer-related genes in solid tumors. We analyzed the promoter methylation status of 6 genes previously reported as cancer-specific methylated (MCAM, SSBP2, NISCH, B4GALT1, KIF1A and RASSF1A) in 38 neural crest-derived tumors by quantitative methylation-specific real-time PCR (QMSP). The results demonstrated that the determination of the methylation status of RASSF1A is able to distinguish between normal and tumor samples in cutaneous melanomas, lung carcinoids and small bowel carcinoids. MCAM methylation levels were significantly higher in lung carcinoids tumors (p=0.001), suggesting that this alteration may represent a molecular biomarker in this tumor type.

scholarly journals Aberrant methylation of EDNRB and p16 genes in hepatocellular carcinoma (HCC) in Taiwan

2006 ◽  
Author(s):  
Li-Sung Hsu ◽  
Hsin-Chen Lee ◽  
Gar-Yang Chau ◽  
Pen-Hui Yin ◽  
Chin-Wen Chi ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Aberrant Methylation

Abstract 193: Dissecting satellite and imprinting genes methylation status in cloned bovine: Aberrant methylation in imprinting loci

2010 ◽  
Author(s):  
Chih-Jie Shen ◽  
Chiao-Chieh Ling ◽  
Perng-Chih Shen ◽  
Winston T. K. Cheng ◽  
Hsiao-Ling Chen ◽  
...  
Keyword(s):  
Methylation Status ◽  
Aberrant Methylation ◽  
Cloned Bovine

scholarly journals Hypermethylation-Associated Silencing of miR-125a and miR-125b: A Potential Marker in Colorectal Cancer

2015 ◽  
Vol 2015 ◽  
pp. 1-7 ◽  
Author(s):  
Hui Chen ◽  
Zhiying Xu
Keyword(s):  
Colorectal Cancer ◽  
Cpg Island ◽  
Methylation Status ◽  
Pcr Analysis ◽  
Aberrant Methylation ◽  
Dna Hypermethylation ◽  
Expression Levels ◽  
Qrt Pcr ◽  
Potential Marker ◽  
Potential Biomarker

Background. MicroRNAs (miRNAs) have been found to be downregulated in human colorectal cancer (CRC), and some of them may function as tumor suppressor genes (TSGs). Aberrant methylation triggers the inactivation of TSGs during tumorigenesis.Patients and Methods. We investigated the methylation status of miR-125 family in CRC tissues and adjacent nontumor tissues by using bisulfite sequencing PCR (BSP). The expression levels of the two miRNAs were determined by quantitative reverse transcription polymerase chain reaction (qRT-PCR).Results. The methylation frequency of miR-125a and miR-125b was higher in CRC tissues. QRT-PCR analysis showed that miR-125a and miR-125b were significantly downregulated in CRC tissues. Moreover, the expression levels of miR-125a and miR-125b were inversely correlated to CpG island methylation in CRC.Conclusions. Our results suggest that DNA hypermethylation may be involved in the inactivation of miR-125a and miR-125b in CRC, and hypermethylation of miR-125 is a potential biomarker for clinical outcome.

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