Oestrogen receptor subtypes in ovarian cancer

2008 ◽  
Author(s):  
Na Wei
BMC Cancer ◽  
2017 ◽  
Vol 17 (1) ◽  
Author(s):  
Karen K. L. Chan ◽  
Michelle K. Y. Siu ◽  
Yu-xin Jiang ◽  
Jing-jing Wang ◽  
Yan Wang ◽  
...  

2008 ◽  
Vol 111 (1) ◽  
pp. 144-151 ◽  
Author(s):  
Karen K. L. Chan ◽  
Na Wei ◽  
Stephanie S. Liu ◽  
Liao Xiao-Yun ◽  
Annie N. Cheung ◽  
...  

2014 ◽  
Vol 26 (7) ◽  
pp. 439-447 ◽  
Author(s):  
L. Zhou ◽  
L. Fester ◽  
S. Haghshenas ◽  
X. de Vrese ◽  
R. von Hacht ◽  
...  

2017 ◽  
Vol 46 (2) ◽  
pp. 723-731 ◽  
Author(s):  
Cai-xia Zhu ◽  
Wei Xiong ◽  
Ma-lie Wang ◽  
Juan Yang ◽  
Hui-juan Shi ◽  
...  

Objective To demonstrate the correlation between nuclear and cytoplasmic G protein-coupled oestrogen receptor (GPR30) expression and clinicopathological features and outcome in patients with ovarian cancer. Methods Nuclear and cytoplasmic GPR30 expressions were determined using immunohistochemistry to identify the intracellular location in tissues from patients with ovarian cancer. Data were correlated with clinicopathological characteristics and outcomes. Results Tissue samples were obtained from 110 patients with epithelial ovarian cancer between 2005 and 2010. Nuclear GPR30 was significantly more frequent in the group of patients with recurrence. The presence of nuclear GPR30 predicted lower overall survival) and 5-year progression-free survival in all patients with ovarian cancer and overall survival in patients with high grade ovarian cancer. Cytoplasmic GPR30 was observed significantly more often in advanced ovarian cancer and did not predict survival. Conclusion This study showed that nuclear GPR30 is an independent negative prognostic indicator in patients with ovarian cancer, especially in those with a high grade malignancy.


2012 ◽  
Vol 24 (1) ◽  
pp. 188
Author(s):  
K.-A Hwang ◽  
S.-H. Hyun ◽  
E.-B. Jeung ◽  
K.-C. Choi

Because endocrine disrupting chemicals may interfere with the endocrine systems of our body and have an oestrogenic activity, we evaluated the effects of bisphenol A (BPA) on the transcriptional levels of altered genes in oestrogen receptor (ER)-positive BG-1 ovarian cancer cells. A microarray and RT-qPCR were employed to detect gene alterations in these cells following treatments. In this study, treatment with 17-β-oestradiol (E2) or BPA increased mRNA levels of E2-responsive genes related to apoptosis, cancer and cell cycle, signal transduction and nucleic acid binding and so on. Parallel with the microarray data, the mRNA levels of some altered genes including RAB31_member RAS oncogene family (U59877), cyclin D1 (X59798), cyclin-dependent kinase 4 (U37022), IGF-binding protein 4 (U20982) and anti-mullerian hormone (NM_000479) were significantly induced by E2 or BPA in this cell model. These results indicate that BPA in parallel with E2 induced the transcriptional levels of E2-responsive genes in an ER-positive BG-1 cells. In conclusion, these microarray and RT-qPCR results indicate that BPA, a potential weak oestrogen, may have an oestrogenic effect by regulating E2-responsive genes in ER-positive BG-1 cells and that BG-1 cells would be the best in vitro model to detect these oestrogenic endocrine disrupting chemicals. This work was supported by the National Research Foundation of Korea (NRF) grant funded by the Korea government (MEST) (No. 2011-0015385).


2015 ◽  
Vol 113 (9) ◽  
pp. 1384-1395 ◽  
Author(s):  
Anushka Dikshit ◽  
Manoel Adrião Gomes Filho ◽  
Erfan Eilati ◽  
Stacey McGee ◽  
Carrie Small ◽  
...  

The objective of the present study was to find the optimum dose of flaxseed that would decrease PG and alter oestrogen pathway endpoints implicated in ovarian cancer. In the study, four groups of fifty 1·5-year-old chickens were fed different amounts of flaxseed (0, 5, 10 or 15 % of their total diet) for 4 months and were then killed to collect blood and tissues. Levels of flaxseed lignan metabolites, Enterolactone (EL) and Enterodiol (ED) were measured in the serum, liver and ovaries by liquid chromatography–MS/MS, and n-3 and n-6 fatty acid (FA) levels were measured by GC. The effects of the varied flaxseed doses were assessed by measuring levels of PGE2 and oestrogen metabolites (16-hydroxyestrone (16-OHE1) and 2-hydroxyestrone (2-OHE1)) as well as by analysing the expression of the oestradiol metabolising enzymes CYP3A4 (cytochrome p450, family 3, subfamily A, polypeptide 4), CYP1B1 (cytochrome p450, family 1, subfamily B, polypeptide 1) and CYP1A1 (cytochrome p450, family 1, subfamily A, polypeptide 1) and that of oestrogen receptor α (ERα) in the ovaries. The ratio of n-3:n-FA increased with an increase in flaxseed supplementation and corresponded to a dose-dependent decrease in cyclo-oxygenase-2 protein and PGE2 levels. EL and ED increased in the serum, liver and ovaries with increased concentrations of flaxseed. Flaxseed decreased the expression of ERα in the ovaries. The ratio of 2-OHE1:16-OHE1 in the serum increased significantly in the 15 % flaxseed diet, and there was a corresponding increase in CYP1A1 in the liver and decrease in CYP3A4 in the ovaries. CYP1B1 mRNA also decreased with flaxseed diet in the ovaries. The 15 % flaxseed-supplemented diet significantly decreased inflammatory PGE2, ERα, CYP3A4, CYP1B1 and 16-OHE1, but it increased CYP1A1 and 2-OHE1, which thus reduced the inflammatory and pro-carcinogenic micro-environment of the ovaries.


Reproduction ◽  
2016 ◽  
Vol 151 (6) ◽  
pp. 693-707 ◽  
Author(s):  
Ghungroo Saraswat ◽  
Rajdeep Guha ◽  
Kalyani Mondal ◽  
Piyali Saha ◽  
Sayani Banerjee ◽  
...  

AbstractPuerarin, a selective oestrogen receptor modulator, intercepts implantation in rats, albeit at unacceptably higher doses. We developed poly lactic-co-glycolic acid-encapsulated nano-puerarin (PN) and mapped the molecular pathway underlying its anti-implantation effects. Smooth-surfaced and spherical PN having a mean diameter of ∼147nm was obtained with good yield, efficient encapsulation, and optimum drug loading. In culture, PN slowly and steadily released puerarin, which was readily taken up by the decidual cells. PN exerted a dose-dependent anti-implantation effect. As marked by attenuated expression of stromal cell desmin, alkaline phosphatase, IGFBP1, and decidual prolactin-related protein, the anti-implantation effect of PN seemed secondary to compromised decidualization. Usingin vivo(pregnant and pseudopregnant rats) andin vitro(endometrial stromal cell culture) treatment models, we document that PN enforced inhibition of uterine expression ofHbegfandHoxa10and their downstream signalling molecules, Cyclin D3 (CCND3)/CDK4. PN also efficiently ablated theIhh-Nr2f2-Bmp2signalling pathway and invited the loss of uterine potential for decidualization. There was a dose-dependent up-regulation of RHOA and its effector protein kinase, ROCK1, leading to the promotion of MLC phosphorylation and actin–myosin interaction. PN also down-regulated the stromal cell activation of ERK½ and expression of MMP9. These effects acting together stabilized the stroma and inhibited the stromal cell migration. Central to this array of events was the adversely altered endometrial expression of oestrogen receptor subtypes and repression of progesterone receptor that indulged endless proliferation of luminal epithelia and distorted the precisely choreographed stroma–epithelia crosstalk. Thus, PN dismantles the endometrial bed preparation and prevents implantation.


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