scholarly journals Promoter Methylation and mRNA Expression of Response Gene to Complement 32 in Breast Carcinoma

2016 ◽  
Vol 2016 ◽  
pp. 1-6 ◽  
Author(s):  
Ebrahim Eskandari-Nasab ◽  
Mohammad Hashemi ◽  
Firoozeh Rafighdoost
Keyword(s):  
Mrna Expression ◽  
Promoter Methylation ◽  
Methylation Status ◽  
Methylation Pattern ◽  
Response Gene ◽  
Expression Levels ◽  
Promoter Methylation Status ◽  
Normal Tissues ◽  
A Cell ◽  
Methylation Patterns

Background. Response gene to complement 32 (RGC32), induced by activation of complements, has been characterized as a cell cycle regulator; however, its role in carcinogenesis is still controversial. In the present study we comparedRGC32promoter methylation patterns and mRNA expression in breast cancerous tissues and adjacent normal tissues.Materials and Methods. Sixty-three breast cancer tissues and 63 adjacent nonneoplastic tissues were included in our study.Design. Nested methylation-specific polymerase chain reaction (Nested-MSP) and quantitative PCR (qPCR) were used to determineRGC32promoter methylation status and its mRNA expression levels, respectively.Results. RGC32 methylation pattern was not different between breast cancerous tissue and adjacent nonneoplastic tissue (OR = 2.30, 95% CI = 0.95–5.54). However, qPCR analysis displayed higher levels ofRGC32mRNA in breast cancerous tissues than in noncancerous tissues (1.073 versus 0.959;P=0.001), irrespective of the promoter methylation status. The expression levels and promoter methylation ofRGC32were not correlated with any of patients’ clinical characteristics (P>0.05).Conclusion. Our findings confirmed upregulation of RGC32 in breast cancerous tumors, but it was not associated with promoter methylation patterns.

scholarly journals Promoter Methylation Status and Expression Levels of RASSF1A Gene in Different Phases of Acute Lymphoblastic Leukemia (ALL)

2021 ◽  
Author(s):  
Mahsa Sohani ◽  
Shahrbano Rostami ◽  
Mehdi Azad ◽  
Tahereh Hojjatipour ◽  
Bahram Chahardouli ◽  
...  
Keyword(s):  
Acute Lymphoblastic Leukemia ◽  
Tumor Suppressor ◽  
Promoter Methylation ◽  
Lymphoblastic Leukemia ◽  
Methylation Status ◽  
Response To Therapy ◽  
Control Group ◽  
Expression Levels ◽  
Promoter Methylation Status ◽  
Control Samples

Background: Although the precise pathogenesis of acute lymphoblastic leukemia (ALL) remains unclear, studying gene-regulating mechanisms during ALL pathogeneses may shed light on the underlying mechanisms driving malignant behavior. There is some evidence showing the promoter hypermethylation and silencing of RASSF1A tumor suppressor gene in ALL cells; however, there is a lack of evidence for whether the gene indeed alters during different phases of ALL or in response to therapy. Thus, the current study aimed to clarify this issue using groups of adult ALL patients who have been scarcely investigated regarding expression levels and promoter methylation status. Materials and Methods: In this case/control study, the expression levels and methylation status of the gene promoter was evaluated using quantitative real-time PCR and methylation-specific PCR (MSP), respectively in adults with ALL. The study included peripheral blood of patients with newly diagnosed ALL (n=10), complete remission (CR) (n=10), or relapse (n=10), and 10 control samples from healthy individuals. Results: MSP results revealed an unmethylated status for almost all patients and control samples, except a case with relapsing ALL, which showed a hemimethylated pattern. RASSF1A also showed no difference in terms of gene expression in the patients compared with the control group (p>0.05). Conclusion: The results revealed an up-regulation of RASSF1A tumor suppressor in adult ALL patients experiencing CR, suggesting this to be a marker of therapy response. However, further investigations using more sensitive methylation detecting tools with larger sample sizes may better clarify the involvement of the promoter methylation of RASSF1A in these patients.  

scholarly journals Correlation of MGMT promoter methylation status with gene and protein expression levels in glioblastoma

Clinics ◽  
2011 ◽  
Vol 66 (10) ◽  
pp. 1747-1755 ◽  
Author(s):  
Miyuki Uno ◽  
Sueli Mieko Oba-Shinjo ◽  
Anamaria Aranha Camargo ◽  
Ricardo Pereira Moura ◽  
Paulo Henrique de Aguiar ◽  
...  
Keyword(s):  
Protein Expression ◽  
Promoter Methylation ◽  
Methylation Status ◽  
Mgmt Promoter Methylation ◽  
Expression Levels ◽  
Promoter Methylation Status ◽  
Gene And Protein Expression ◽  
Mgmt Promoter ◽  
Mgmt Promoter Methylation Status

Evaluation of mir-203 Expression Levels and DNA Promoter Methylation Status in Serum of Patients with Endometrial Cancer

2017 ◽  
Vol 63 (10/2017) ◽  
Author(s):  
Marco Benati ◽  
Martina Montagnana ◽  
Elisa Danese ◽  
Elisa Paviati ◽  
Silvia Giudici ◽  
...  
Keyword(s):  
Endometrial Cancer ◽  
Promoter Methylation ◽  
Methylation Status ◽  
Expression Levels ◽  
Promoter Methylation Status

Promoter Methylation Status in Pro-opiomelanocortin Does Not Contribute to Dyspigmentation in Hypertrophic Scar

2019 ◽  
Author(s):  
Bonnie C Carney ◽  
Ryan D Dougherty ◽  
Lauren T Moffatt ◽  
Cynthia M Simbulan-Rosenthal ◽  
Jeffrey W Shupp ◽  
...  
Keyword(s):  
Protein Expression ◽  
Promoter Methylation ◽  
Normal Skin ◽  
Methylation Status ◽  
Cpg Islands ◽  
Treatment Strategies ◽  
Gene Promoter ◽  
Promoter Methylation Status ◽  
Pomc Gene ◽  
Methylation Patterns

Abstract Burn injuries frequently result in hypertrophic scars (HTSs), specifically when excision and grafting are delayed due to limited resources or patient complications. In patient populations with dark baseline pigmentation, one symptom of HTS that often occurs is dyspigmentation. The mechanism behind dyspigmentation has not been explored, and, as such, prevention and treatment strategies for this morbidity are lacking. The mechanism by which cells make pigment is controlled at the apex of the pathway by pro-opiomelanocortin (POMC), which is cleaved to its products alpha-melanocyte-stimulating hormone (α-MSH) and adrenocorticotropin hormone (ACTH). α-MSH and ACTH secreted by keratinocytes bind to melanocortin 1 receptor (MC1R), expressed on melanocytes, to initiate melanogenesis. POMC protein expression is upregulated in hyperpigmented scar compared to hypopigmented scar by an unknown mechanism in a Duroc pig model of HTS. POMC RNA levels, as well as the POMC gene promoter methylation status were investigated as a possible mechanism. DNA was isolated from biopsies obtained from distinct areas of hyper- or hypopigmented scar and normal skin. DNA was bisulfite-converted, and amplified using two sets of primers to observe methylation patterns in two different CpG islands near the POMC promoter. Amplicons were then sequenced and methylation patterns were evaluated. POMC gene expression was significantly downregulated in hypopigmented scar compared to normal skin, consistent with previously reported protein expression levels. There were significant changes in methylation of the POMC promoter; however, none that would account for the development of hyper- or hypopigmentation. Future work will focus on other areas of POMC transcriptional regulation.

scholarly journals Prognostic Value Estimation of BRIP1 in Breast Cancer by Exploiting Transcriptomics Data Through Bioinformatics Approaches

2021 ◽  
Vol 15 ◽  
pp. 117793222110558
Author(s):  
Umama Khan ◽  
Md. Salauddin Khan
Keyword(s):  
Breast Cancer ◽  
Clinical Features ◽  
Promoter Methylation ◽  
Breast Tumor ◽  
Prognostic Value ◽  
Methylation Status ◽  
Promoter Methylation Status ◽  
Tumor Subtypes ◽  
Normal Tissues ◽  
Brip1 Gene

BRIP1 (Breast Cancer 1 Interacting Helicase 1) is a tumor suppressor gene that has vital function in preserving the genetic stability by repairing DNA damage though have significant associations with the onset of breast cancer (BC) if mutated or overexpressed. In this study, the prognostic value of BRIP1 gene was evaluated and validated through bioinformatics approaches utilizing transcriptomic (mRNA expression) data from several BC databases. To determine the prognostic value, the expression level of mRNA transcript was analyzed in context of comparison between breast tumor and normal tissues regarding clinical features, breast tumor subtypes, promoter methylation status, correlation level, mutation frequency, and survival of BC patients. BRIP1 expression was found to be significantly overexpressed in various BC molecular subtypes (e.g. PAM50, Sorlie’s) and clinical status (estrogen and progesterone receptor) than associated normal tissues which correlated with prognosis. Also, in promoter methylation level, its expression was observed as upregulated-hypomethylated regarding various clinicopathological features. Multiple data mining exhibited positive correlation between BRIP1 and INTS2 (Integrator Complex Subunit 2) expressions in BC. Further, mutation analysis revealed that BRIP1 gene was altered by acquiring both somatic and germline mutations. In addition, a total of 42 mutations; 24 missense, 8 fusion, 7 truncating, and 3 inframe mutations in BC patients was detected in BRIP1 protein. Moreover, higher BRIP1 expression was found to be correlated with poor disease-specific, disease metastasis-free, relapse-free, and overall survivals of BC patients. Since, overexpression of BRIP1 was identified to be associated with different clinical features, breast tumor subtypes, promoter methylation status, and survival of BC patients that may provide a risk of ensuing malignant transformation. Thus, lower expression of BRIP1 might hinder BC prognosis. We consider that this analysis will present a proof for BRIP1 gene to be a noteworthy molecular biomarker for BC prognosis.

Sign in / Sign up

Export Citation Format

Share Document