Analyzing genetic and epigenetic HORMAD alterations in  breast cancer resistance and metastatic events

N.A.

Makale detayları

Analyzing genetic and epigenetic HORMAD alterations in breast cancer resistance and metastatic events

Yazarlar:

N.A.

Yayıncı:

Marmara University

Ana Başlıklar:

Pharmacology and Pharmaceutical Sciences (Other)

Dergi:

Journal of Research in Pharmacy Vol.29 Issue 1, pp.137-150

Belge Tipi:

Makale

Yayın Tarihi:

3/2025

Belge Dili:

İngilizce

Document ID (Org No.):

2001339600

pISSN:

2630-6344

Anahtar kelimeler:

Özet:

 Epigenetic alterations in regulatory genes, genetic factors, and genomic instability, which cause breast cancer, can also contribute to disease resistance. HORMAD , which encode proteins containing HORMA domains and are involved in homologous recombination, have important roles in cancer emergence and progression. In this study, we uncovered putative breast cancer therapeutic targets by examining HORMAD1 and HORMAD2 genetic and epigenetic alterations. mRNA levels of HORMAD1 and HORMAD2 in breast cancer samples and normal breast tissues, as well as mRNA levels in normal, breast cancer, and metastatic breast cancer samples, were analyzed using TNMplot. Prognostic value, genetic alterations, epigenetic alterations, genetic variations, ROC plots, functional prediction, and immune infiltration of HORMAD1 and HORMAD2 were conducted with KMPlotter, cBioportal, methsurv, ClinVar, ROC Plotter, PredictSNP, PANTHER, and TIMER 2.0, respectively. Both HORMAD1 and HORMAD2 mRNA levels were lower in breast cancer samples, and lower in metastatic breast cancer samples. Patients expressing higher HORMAD1 and HORMAD2 levels had favorable overall survival OS rates than the opposite groups. HORMAD1 and HORMAD2 gene amplifications and deletions were also observed. Pathway enrichment analyses showed that Wnt signaling alterations contributed to cell proliferation. Increased DNA methylation levels were identified in HORMAD2 when compared with HORMAD1 in patients. Two 1021CT Q334 and 430AG T144A variants of HORMAD1 were shown to have clinical significance in patients. Also, functional prediction mutant analysis of HORMAD1 confirmed that S287F exerted a deleterious effect on amino acid impact, however, further investigations are warranted. Receiver operating characteristic ROC plot data indicated a significant correlation between HORMAD2 levels and anti-human epidermal growth factor receptor 2 HER2 sensitivity. Genetic and epigenetic changes in HORMAD1 and HORMAD2 genes may be used as indicators and targets for overcoming breast cancer resistance and limiting metastasis in breast cancer cells via Wnt targeting. Further research is required to verify our findings.

 Epigenetic alterations in regulatory genes, genetic factors, and genomic instability, which cause breast cancer, can also contribute to disease resistance. HORMAD , which encode proteins containing HORMA domains and are involved in homologous recombination, have important roles in cancer emergence and progression. In this study, we uncovered putative breast cancer therapeutic targets by examining HORMAD1 and HORMAD2 genetic and epigenetic alterations. mRNA levels of HORMAD1 and HORMAD2 in breast cancer samples and normal breast tissues, as well as mRNA levels in normal, breast cancer, and metastatic breast cancer samples, were analyzed using TNMplot. Prognostic value, genetic alterations, epigenetic alterations, genetic variations, ROC plots, functional prediction, and immune infiltration of HORMAD1 and HORMAD2 were conducted with KMPlotter, cBioportal, methsurv, ClinVar, ROC Plotter, PredictSNP, PANTHER, and TIMER 2.0, respectively. Both HORMAD1 and HORMAD2 mRNA levels were lower in breast cancer samples, and lower in metastatic breast cancer samples. Patients expressing higher HORMAD1 and HORMAD2 levels had favorable overall survival OS rates than the opposite groups. HORMAD1 and HORMAD2 gene amplifications and deletions were also observed. Pathway enrichment analyses showed that Wnt signaling alterations contributed to cell proliferation. Increased DNA methylation levels were identified in HORMAD2 when compared with HORMAD1 in patients. Two 1021CT Q334 and 430AG T144A variants of HORMAD1 were shown to have clinical significance in patients. Also, functional prediction mutant analysis of HORMAD1 confirmed that S287F exerted a deleterious effect on amino acid impact, however, further investigations are warranted. Receiver operating characteristic ROC plot data indicated a significant correlation between HORMAD2 levels and anti-human epidermal growth factor receptor 2 HER2 sensitivity. Genetic and epigenetic changes in HORMAD1 and HORMAD2 genes may be used as indicators and targets for overcoming breast cancer resistance and limiting metastasis in breast cancer cells via Wnt targeting. Further research is required to verify our findings.

 Epigenetic alterations in regulatory genes, genetic factors, and genomic instability, which cause breast cancer, can also contribute to disease resistance. HORMAD , which encode proteins containing HORMA domains and are involved in homologous recombination, have important roles in cancer emergence and progression. In this study, we uncovered putative breast cancer therapeutic targets by examining HORMAD1 and HORMAD2 genetic and epigenetic alterations. mRNA levels of HORMAD1 and HORMAD2 in breast cancer samples and normal breast tissues, as well as mRNA levels in normal, breast cancer, and metastatic breast cancer samples, were analyzed using TNMplot. Prognostic value, genetic alterations, epigenetic alterations, genetic variations, ROC plots, functional prediction, and immune infiltration of HORMAD1 and HORMAD2 were conducted with KMPlotter, cBioportal, methsurv, ClinVar, ROC Plotter, PredictSNP, PANTHER, and TIMER 2.0, respectively. Both HORMAD1 and HORMAD2 mRNA levels were lower in breast cancer samples, and lower in metastatic breast cancer samples. Patients expressing higher HORMAD1 and HORMAD2 levels had favorable overall survival OS rates than the opposite groups. HORMAD1 and HORMAD2 gene amplifications and deletions were also observed. Pathway enrichment analyses showed that Wnt signaling alterations contributed to cell proliferation. Increased DNA methylation levels were identified in HORMAD2 when compared with HORMAD1 in patients. Two 1021CT Q334 and 430AG T144A variants of HORMAD1 were shown to have clinical significance in patients. Also, functional prediction mutant analysis of HORMAD1 confirmed that S287F exerted a deleterious effect on amino acid impact, however, further investigations are warranted. Receiver operating characteristic ROC plot data indicated a significant correlation between HORMAD2 levels and anti-human epidermal growth factor receptor 2 HER2 sensitivity. Genetic and epigenetic changes in HORMAD1 and HORMAD2 genes may be used as indicators and targets for overcoming breast cancer resistance and limiting metastasis in breast cancer cells via Wnt targeting. Further research is required to verify our findings.

 Epigenetic alterations in regulatory genes, genetic factors, and genomic instability, which cause breast cancer, can also contribute to disease resistance. HORMAD , which encode proteins containing HORMA domains and are involved in homologous recombination, have important roles in cancer emergence and progression. In this study, we uncovered putative breast cancer therapeutic targets by examining HORMAD1 and HORMAD2 genetic and epigenetic alterations. mRNA levels of HORMAD1 and HORMAD2 in breast cancer samples and normal breast tissues, as well as mRNA levels in normal, breast cancer, and metastatic breast cancer samples, were analyzed using TNMplot. Prognostic value, genetic alterations, epigenetic alterations, genetic variations, ROC plots, functional prediction, and immune infiltration of HORMAD1 and HORMAD2 were conducted with KMPlotter, cBioportal, methsurv, ClinVar, ROC Plotter, PredictSNP, PANTHER, and TIMER 2.0, respectively. Both HORMAD1 and HORMAD2 mRNA levels were lower in breast cancer samples, and lower in metastatic breast cancer samples. Patients expressing higher HORMAD1 and HORMAD2 levels had favorable overall survival OS rates than the opposite groups. HORMAD1 and HORMAD2 gene amplifications and deletions were also observed. Pathway enrichment analyses showed that Wnt signaling alterations contributed to cell proliferation. Increased DNA methylation levels were identified in HORMAD2 when compared with HORMAD1 in patients. Two 1021CT Q334 and 430AG T144A variants of HORMAD1 were shown to have clinical significance in patients. Also, functional prediction mutant analysis of HORMAD1 confirmed that S287F exerted a deleterious effect on amino acid impact, however, further investigations are warranted. Receiver operating characteristic ROC plot data indicated a significant correlation between HORMAD2 levels and anti-human epidermal growth factor receptor 2 HER2 sensitivity. Genetic and epigenetic changes in HORMAD1 and HORMAD2 genes may be used as indicators and targets for overcoming breast cancer resistance and limiting metastasis in breast cancer cells via Wnt targeting. Further research is required to verify our findings.

Makale detayları

Analyzing genetic and epigenetic HORMAD alterations in breast cancer resistance and metastatic events

Yazarlar:

N.A.

Yayıncı:

Marmara University

Ana Başlıklar:

Pharmacology and Pharmaceutical Sciences (Other)

Dergi:

Journal of Research in Pharmacy Vol.29 Issue 1, pp.137-150

Belge Tipi:

Makale

Yayın Tarihi:

3/2025

Belge Dili:

İngilizce

Document ID (Org No.):

2001339600

pISSN:

2630-6344

HORMAD

breast cancer resistance

metastasis

bioinformatics

genetic and epigenetic alterations

Sayı

Makale detayları

Analyzing genetic and epigenetic HORMAD alterations in breast cancer resistance and metastatic events

Yazarlar: N.A.

Yayıncı: Marmara University

Ana Başlıklar: Pharmacology and Pharmaceutical Sciences (Other)

Dergi: Journal of Research in Pharmacy Vol.29 Issue 1, pp.137-150

Belge Tipi: Makale

Yayın Tarihi: 3/2025

Belge Dili: İngilizce

Document ID (Org No.): 2001339600

pISSN: 2630-6344

HORMAD

breast cancer resistance

metastasis

bioinformatics

genetic and epigenetic alterations

Sayı

Yazarlar:

N.A.

Yayıncı:

Marmara University

Ana Başlıklar:

Pharmacology and Pharmaceutical Sciences (Other)

Dergi:

Journal of Research in Pharmacy Vol.29 Issue 1, pp.137-150

Belge Tipi:

Makale

Yayın Tarihi:

3/2025

Belge Dili:

İngilizce

Document ID (Org No.):

2001339600

pISSN:

2630-6344