gene methylation
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2022 ◽  
Vol 12 (1) ◽  
pp. 159-166
Author(s):  
Ningxiao Wen

The aim of this study was to discover the influence of Neurotrophin receptor-interacting MAGE homolog (NRAGE) gene methylation on proliferation (Pro) and apoptosis (Apo) of breast cancer cell (BCC), and its influence on TrkA/MEK/ERK signaling. BCC lines MCF-7, MDA-MB-231, and normal mammary gland cell (MGC) MCF-10 were selected. Expression of NRAGE mRNA and methylation level in cells was analyzed via reverse transcription-polymerase chain reaction (RT-PCR) and methylation-specific PCR. Different concentrations (0, 5, 10 mol/L) of DNA methylase inhibitor 5-aza-2′-deoxycytidine (5-Aza-CdR) were adopted to treat the BCC cell line. With dimethyl sulfoxide (DMSO) treatment as control, cell count, 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, flow cytometry, and Western blot were adopted to detect the Pro, Apo, relative expression (REP) of Apo-related proteins Bcl-2, Bax, and target proteins TrkA, MEK, and ERK1/2 after different treatments. The results showed that NRAGE mRNA level in MDA-MB-231 and MCF-7 was notably reduced versus MCF-10 (P < 0.05), and they could express methylated NRAGE specifically. 5-Aza-CdR can increase unmethylated NRAGE’s expression in BCC. Cell Pro level of the 5 and 10 mol/L treatments was greatly inhibited than DMSO and 0 mol/L treatments (P < 0.05). Apo rate and Apo-related proteins Bcl-2 and Bax increased obviously (P < 0.05). In addition, the phosphorylation levels of TrkA in the 5 and 10 mol/L treatments were considerably reduced (P < 0.05), while that in MEK and ERK1/2 was remarkably increased (P < 0.05). In short, NRAGE methylation can inhibit BCC’s Pro and regulate BCC’s Pro and Apo through TrkA/MEK/ERK signaling.


PLoS ONE ◽  
2021 ◽  
Vol 16 (12) ◽  
pp. e0260857
Author(s):  
Erin M. Siegel ◽  
Abidemi Ajidahun ◽  
Anders Berglund ◽  
Whitney Guerrero ◽  
Steven Eschrich ◽  
...  

HPV infection results in changes in host gene methylation which, in turn, are thought to contribute to the neoplastic progression of HPV-associated cancers. The objective of this study was to identify joint and disease-specific genome-wide methylation changes in anal and cervical cancer as well as changes in high-grade pre-neoplastic lesions. Formalin-fixed paraffin-embedded (FFPE) anal tissues (n = 143; 99% HPV+) and fresh frozen cervical tissues (n = 28; 100% HPV+) underwent microdissection, DNA extraction, HPV genotyping, bisulfite modification, DNA restoration (FFPE) and analysis by the Illumina HumanMethylation450 Array. Differentially methylated regions (DMR; t test q<0.01, 3 consecutive significant CpG probes and mean Δβ methylation value>0.3) were compared between normal and cancer specimens in partial least squares (PLS) models and then used to classify anal or cervical intraepithelial neoplasia-3 (AIN3/CIN3). In AC, an 84-gene PLS signature (355 significant probes) differentiated normal anal mucosa (NM; n = 9) from AC (n = 121) while a 36-gene PLS signature (173 significant probes) differentiated normal cervical epithelium (n = 10) from CC (n = 9). The CC progression signature was validated using three independent publicly available datasets (n = 424 cases). The AC and CC progression PLS signatures were interchangeable in segregating normal, AIN3/CIN3 and AC and CC and were found to include 17 common overlapping hypermethylated genes. Moreover, these signatures segregated AIN3/CIN3 lesions similarly into cancer-like and normal-like categories. Distinct methylation changes occur across the genome during the progression of AC and CC with overall similar profiles and add to the evidence suggesting that HPV-driven oncogenesis may result in similar non-random methylomic events. Our findings may lead to identification of potential epigenetic drivers of HPV-associated cancers and also, of potential markers to identify higher risk pre-cancerous lesions.


2021 ◽  
Vol 8 (12) ◽  
Author(s):  
Daniel J. Lawson ◽  
Vinesh Solanki ◽  
Igor Yanovich ◽  
Johannes Dellert ◽  
Damian Ruck ◽  
...  

Integrating datasets from different disciplines is hard because the data are often qualitatively different in meaning, scale and reliability. When two datasets describe the same entities, many scientific questions can be phrased around whether the (dis)similarities between entities are conserved across such different data. Our method, CLARITY, quantifies consistency across datasets, identifies where inconsistencies arise and aids in their interpretation. We illustrate this using three diverse comparisons: gene methylation versus expression, evolution of language sounds versus word use, and country-level economic metrics versus cultural beliefs. The non-parametric approach is robust to noise and differences in scaling, and makes only weak assumptions about how the data were generated. It operates by decomposing similarities into two components: a ‘structural’ component analogous to a clustering, and an underlying ‘relationship’ between those structures. This allows a ‘structural comparison’ between two similarity matrices using their predictability from ‘structure’. Significance is assessed with the help of re-sampling appropriate for each dataset. The software, CLARITY, is available as an R package from github.com/danjlawson/CLARITY .


2021 ◽  
pp. 105629
Author(s):  
Hannah Spencer ◽  
Franca H. Parianen Lesemann ◽  
Eline J. Kraaijenvanger ◽  
Geertjan Overbeek ◽  
Estrella R. Montoya ◽  
...  
Keyword(s):  

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Xiaoping Wang ◽  
Ping Guo ◽  
Jiahui Tian ◽  
Jie Li ◽  
Na Yan ◽  
...  

Abstract Background LncRNA GAS5 and miR-155 are reported to play opposite roles in lung inflammatory responses. Lung inflammation participates in childhood pneumonia, indicating the involvement of GAS5 and miR-155 in pneumonia. The study aimed to analyze the potential interaction between GAS5 and miR-155 in childhood pneumonia. Methods GAS5 and miR-155 levels in plasma samples from pneumonia patients and controls were detected using RT-qPCR. The role of GAS5 in miR-155 RNA gene methylation in human bronchial epithelial cells (HBEpCs) was analyzed by methylation analysis. Flow cytometry and RT-qPCR were applied to analyze cell apoptosis and SHIP-1 expression, respectively. Results GAS5 was downregulated in pneumonia, and miR-155 was upregulated in pneumonia. GAS5 and miR-155 were inversely correlated. GAS5 overexpression decreased miR-155 expression in HBEpCs, while miR-155 overexpression showed no significant effects on GAS5 expression. In addition, GAS5 suppressed LPS-induced HBEpC apoptosis, promoted SHIP-1 expression, and reduced the enhancing effect of miR-155 on cell apoptosis and SHIP-1 expression. Conclusions GAS5 may participate in childhood pneumonia by inhibiting cell apoptosis and promoting SHIP-1 expression via downregulating miR-155.


Cancers ◽  
2021 ◽  
Vol 13 (21) ◽  
pp. 5491
Author(s):  
George I. Lambrou ◽  
Myrto Poulou ◽  
Krinio Giannikou ◽  
Marios Themistocleous ◽  
Apostolos Zaravinos ◽  
...  

Epigenetic modifications are considered of utmost significance for tumor ontogenesis and progression. Especially, it has been found that miRNA expression, as well as DNA methylation plays a significant role in central nervous system tumors during childhood. A total of 49 resected brain tumors from children were used for further analysis. DNA methylation was identified with methylation-specific MLPA and, in particular, for the tumor suppressor genes CASP8, RASSF1, MGMT, MSH6, GATA5, ATM1, TP53, and CADM1. miRNAs were identified with microarray screening, as well as selected samples, were tested for their mRNA expression levels. CASP8, RASSF1 were the most frequently methylated genes in all tumor samples. Simultaneous methylation of genes manifested significant results with respect to tumor staging, tumor type, and the differentiation of tumor and control samples. There was no significant dependence observed with the methylation of one gene promoter, rather with the simultaneous presence of all detected methylated genes’ promoters. miRNA expression was found to be correlated to gene methylation. Epigenetic regulation appears to be of major importance in tumor progression and pathophysiology, making it an imperative field of study.


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