scholarly journals Oestrogen receptors and antioestrogen treatment of hormone-dependent tumours

2018 ◽  
Vol 49 (2) ◽  
pp. 91
Author(s):  
N. G. KOSTOMITSOPOULOS (Ν.Γ. ΚΩΣΤΟΜΗΤΣΟΠΟΥΛΟΣ)
Keyword(s):  
Breast Cancer ◽  
Gene Expression ◽  
Dna Sequences ◽  
Human Breast Cancer ◽  
Oestrogen Receptor ◽  
Specific Gene ◽  
Oestrogen Receptors ◽  
Human Breast ◽  
Potential Use

The oestrogen receptor is a ligand-activated transcription factor that modulates specific gene expression by binding to short DNA sequences. The study of the role of oestrogen receptor on the expression of the mitogenic actionof oestrogens and oncogenesis lead biomedical research in new approaches of the treatment of oestrogen-dependent tumors by using antioestrogens. Main mechanism of action of antioestrogens is the prevention of oestrogen action by blocking the binding of oestradiol to the oestrogen receptor. Tamoxifen, the most wellknown antioestrogen, is widely used as adjuvant therapy in all stages of human breast cancer. Recently interest is focused on the potential use of "pure" antioestrogens. The use of antioestrogens in veterinary oncology is also under discussion.

scholarly journals Low E2F2 activity is associated with high genomic instability and PARPi resistance

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Jonathan P. Rennhack ◽  
Eran R. Andrechek
Keyword(s):  
Breast Cancer ◽  
Gene Expression ◽  
Cell Cycle ◽  
Dna Repair ◽  
Human Breast Cancer ◽  
Metabolic Reprogramming ◽  
Patient Treatment ◽  
Expression Data ◽  
Human Breast

Abstract The E2F family, classically known for a central role in cell cycle, has a number of emerging roles in cancer including angiogenesis, metabolic reprogramming, metastasis and DNA repair. E2F1 specifically has been shown to be a critical mediator of DNA repair; however, little is known about DNA repair and other E2F family members. Here we present an integrative bioinformatic and high throughput drug screening study to define the role of E2F2 in maintaining genomic integrity in breast cancer. We utilized in vitro E2F2 ChIP-chip and over expression data to identify transcriptional targets of E2F2. This data was integrated with gene expression from E2F2 knockout tumors in an MMTV-Neu background. Finally, this data was compared to human datasets to identify conserved roles of E2F2 in human breast cancer through the TCGA breast cancer, Cancer Cell Line Encyclopedia, and CancerRx datasets. Through these methods we predict that E2F2 transcriptionally regulates mediators of DNA repair. Our gene expression data supports this hypothesis and low E2F2 activity is associated with a highly unstable tumor. In human breast cancer E2F2, status was also correlated with a patient’s response to PARP inhibition therapy. Taken together this manuscript defines a novel role of E2F2 in cancer progression beyond cell cycle and could impact patient treatment.

Long non-coding RNA PVT1 regulates the proliferation and metastasis of human breast cancer via the Wnt/b-catenin signalling pathway

2021 ◽  
Author(s):  
Nianqu Zhang ◽  
Qing Li ◽  
Shanmei Sun
Keyword(s):  
Breast Cancer ◽  
Gene Expression ◽  
Cell Death ◽  
Cancer Cells ◽  
Human Breast Cancer ◽  
Apoptotic Cell ◽  
Migration And Invasion ◽  
Human Breast ◽  
Gene Expression Levels

IntroductionThe development of many human diseases has been implicated to be coupled by the dysregulation of long non-coding RNAs (lncRNAs). Considering this, the current study was aimed at identifying and then investigating the molecular role of a specific lncRNA from a set of such genetic elements in regulating the developmental aspects of human breast cancer.Material and methodsThe quantitative real-time polymerase chain reaction (qRT-PCR) method was used to deduce the gene expression levels. Proliferation of cancer cells was determined by the cell counting kit 8 (CCK8). The evaluation of apoptotic cell death in breast cancer cells was made through the acridine orange/ethidium bromide (AO/EB) and annexin V-FITC staining protocols. Transwell assays were used to monitor cell migration and invasion.ResultsEstimation of gene expression levels of a set of lncRNAs showed that lncRNA PVT1 is specifically overexpressed in the breast cancer tissues and cell lines. The downregulation of PVT1 in cancer cells negatively affected their proliferation rates, and cancer cells exhibited significantly lower viabilities due to induction of Bax/Bcl-2 signal arbitrated apoptotic cell death in the cancer cells. Moreover, the cancer cells showed significantly lower rates of migration and invasion when lncRNA PVT1 was repressed. The PVT1 repression-driven anti-cancer effects against the cancer cells were seen to be modulated through the Wnt/β-catenin signalling pathway.ConclusionsThe results of this work are indicative of the prognostic role of lncRNA PVT1 in breast cancer. Also, the molecular targeting of PVT1 might prove to be a vital step against the progression of human breast cancer.

scholarly journals The role of YY1 in reduced HP1α gene expression in invasive human breast cancer cells

2009 ◽  
Vol 11 (3) ◽  
Author(s):  
Jason G Lieberthal ◽  
Marissa Kaminsky ◽  
Christopher N Parkhurst ◽  
Naoko Tanese
Keyword(s):  
Breast Cancer ◽  
Gene Expression ◽  
Cancer Cells ◽  
Human Breast Cancer ◽  
Breast Cancer Cells ◽  
Human Breast Cancer Cells ◽  
Human Breast ◽  
Invasive Human Breast Cancer

scholarly journals Oestrogen receptor alpha increases p21(WAF1/CIP1) gene expression and the antiproliferative activity of histone deacetylase inhibitors in human breast cancer cells

2003 ◽  
Vol 179 (1) ◽  
pp. 41-53 ◽  
Author(s):  
R Margueron ◽  
A Licznar ◽  
G Lazennec ◽  
F Vignon ◽  
V Cavailles
Keyword(s):  
Breast Cancer ◽  
Gene Expression ◽  
Cancer Cells ◽  
Histone Deacetylase ◽  
Human Breast Cancer ◽  
Oestrogen Receptor ◽  
Breast Cancer Cells ◽  
Human Breast Cancer Cells ◽  
Human Breast ◽  
P21 Waf1

We analysed the antiproliferative activity of various histone deacetylase (HDAC) inhibitors such as trichostatin A (TSA) on human breast cancer cells. We observed a lower sensitivity to HDAC inhibition for oestrogen receptor negative (ER-) versus positive (ER+) cell lines. This differential response was associated neither with a modification of drug efflux via the multidrug resistance system nor with a global modification of histone acetyltransferase (HAT)/HDAC activities. In contrast, we demonstrated that in ER+ breast cancer cells the p21(WAF1/CIP1) gene was more sensitive to TSA regulation and was expressed at higher levels. These differences were observed both in transient transfection experiments and on the endogenous p21(WAF1/CIP1) gene. The Sp1 transcription factor, which was shown to interact in vitro with both class I and class II HDACs, is sufficient to confer the differential sensitivity to TSA and participated in the control of p21(WAF1/CIP1) basal expression. Finally, re-expression of ERalpha following adenoviral infection of ER- breast cancer cells increased both p21(WAF1/CIP1) protein accumulation and the growth inhibitory activity of TSA. Altogether, our results highlight the key role of ERalpha and p21(WAF1/CIP1) gene expression in the sensitivity of breast cancer cells to hyperacetylating agents.

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