Oestrogen induced downregulation of TFPI expression is mediated by ERα

Ali, Huda Omar; Stavik, Benedicte; Dørum, E.; Iversen, Nina; Sandset, Per Morten; Skretting, Grethe

doi:10.1016/j.thromres.2014.04.004

Cited by 16 publications

(12 citation statements)

References 43 publications

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“…S3), suggesting that the net increase of FXa generation in the case of miR‐27a/b may be due to a miRNA‐mediated downregulation of TFPIα. We also observed a similar observation in estrogen‐mediated downregulation of TFPIα in MCF7 cells . In miR‐494 transfected cells, however, the higher FXa generation observed may be a combined effect of TF induction and the reduction of TFPIα.…”

Section: Discussionsupporting

confidence: 84%

“…Estrogens have previously been reported to reduce TFPIα protein secretion in human endothelial cell cultures , but no marked reduction of TFPI mRNA levels was detected in these cells. We have, however, recently reported that the estrogen receptor ligands E2 and EE2 lead to significant reduction of TFPI mRNA and protein levels in MCF7 cells, a process that was mediated through ERα . Observations from our laboratory indicated that both isoforms of TFPI were downregulated by EE2 treatment, although the effect was most evident in the TFPIα isoform (Fig.…”

Section: Discussionmentioning

confidence: 84%

“…Using isoform‐specific TaqMan assays against TFPI showed a more pronounced downregulation of the TFPI mRNA translating the TFPIα isoform (H. O. Ali, unpublished observations). Moreover, because estrogens reduce TFPI expression and low TFPI expression has been associated with increased growth of breast cancer cells , it can be correlated with the estrogen‐mediated induction of miR‐27a/b that negatively regulated TFPIα in MCF7 cells. These findings may suggest the induction of miR‐27a/b by estrogens as a possible contributing factor for the higher risk of breast cancer in patients taking HT.…”

Section: Discussionmentioning

confidence: 99%

“…Estrogens affect breast cancer cells usually through ligand‐dependent nuclear receptors, such as estrogen receptor alpha (ERα) . Recently, we reported that estrogens downregulated TFPI at the transcriptional level in the breast cancer cell line MCF7 , an effect mediated through ERα. Additionally, accumulating evidence indicates that estrogen‐activated ERα signaling may modulate the expression of target genes indirectly by regulating microRNA (miRNA) expression .…”

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confidence: 99%

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The role of microRNA‐27a/b and microRNA‐494 in estrogen‐mediated downregulation of tissue factor pathway inhibitor α

Ali

Arroyo

Gónzález-Conejero

et al. 2016

Journal of Thrombosis and Haemostasis

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To cite this article: Ali HO, Arroyo AB, Gonz alez-Conejero R, Stavik B, Iversen N, Sandset PM, Mart ınez C, Skretting G. The role of microRNA27a/b and microRNA-494 in estrogen-mediated downregulation of tissue factor pathway inhibitor a. J Thromb Haemost 2016; 14: 1226-37. Essentials• Estrogens are known to influence the expression of microRNAs in breast cancer cells.• We looked at microRNAs in estrogenic regulation of tissue factor pathway inhibitor a (TFPIa).• Estrogen upregulated microRNA-27a/b and micro-RNA-494 through the estrogen receptor a.• MicroRNA-27a/b and microRNA-494 are partly involved in estrogenic downregulation of TFPIa.Summary. Background: Tissue factor pathway inhibitor (TFPI) has been linked to breast cancer pathogenesis. We have recently reported TFPI mRNA levels to be downregulated by estrogens in a breast cancer cell line (MCF7) through the estrogen receptor a (ERa). Accumulating evidence also indicates that activation of ERa signaling by estrogens may modulate the expression of target genes indirectly through microRNAs (miRNAs) .

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Section: Discussionsupporting

confidence: 84%

Section: Discussionmentioning

confidence: 84%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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The role of microRNA‐27a/b and microRNA‐494 in estrogen‐mediated downregulation of tissue factor pathway inhibitor α

Ali

Arroyo

Gónzález-Conejero

et al. 2016

Journal of Thrombosis and Haemostasis

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“…The VTE risk in women using COC is attributed to changes in hemostasis . We know that estrogen increases gene expression as well as plasma levels of coagulation factors, and decreases anticoagulant factors such as protein S and a tissue factor pathway inhibitor . In contrast, progestin stimulates the gene expression of protein S …”

Section: Introductionmentioning

confidence: 99%

Risks of thromboembolism associated with hormone contraceptives in Japanese compared with Western women

Kobayashi

Sugiura

Ojima

2017

J of Obstet and Gynaecol

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We extracted 581 thromboembolic events associated with combined oral contraceptives (COC) that occurred between 2004 and 2013 in Japan, from the Pharmaceuticals and Medical Devices Agency database. The most common thromboembolic events associated with COC were deep vein thrombosis, pulmonary embolism and their combination. The reported thromboembolic events increased year by year, in association with an increase in the quantity of prescribed low-dose estrogen progestin after approval for health insurance coverage for dysmenorrhea in 2008 in Japan. The incidence of venous thromboembolism (VTE) in Japanese COC users is estimated to be lower compared with their Western counterparts. In contrast, the frequency of all thromboembolic events peaked at 90 days from the start of COC, as in Western studies. The risk of VTE in the overweight group (body mass index ≥ 25 kg/m 2 ) was more than twofold higher than in the standard group, and age-specific incidence rate rose sharply after the age of 40. There were different VTE risks according to progestin type in Japan as in Western countries, but a definite conclusion about risk according to progestin type was not able to be reached at present. As for the risk of arterial embolism and thrombosis, the difference by progestin type was small, but it became higher at ≥50 years of age. Last, mortality rate caused by thromboembolism is extremely low among COC users.

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