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

Ali, Huda Omar; Arroyo, Ana B.; Gónzález-Conejero, Rocío; Stavik, Benedicte; Iversen, Nina; Pm, Sandset; Martı́nez, Constantino; Skretting, Grethe

doi:10.1111/jth.13321

Cited by 32 publications

(18 citation statements)

References 51 publications

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“…It was demonstrated that exosomal miRNA‐155, an onco‐miRNA, inhibits SOCS6, can activate STAT3 and elevate the expression of the genes involved in proliferation and differentiation of SKBR3 cells and MCF‐7, finally leading to resistance of BC cells to tamoxifen . Some studies reported that miRNA‐27a/b negatively affects the expression of TFPIa in MCF‐7 cells . TFPIa is an apoptosis inducer in BC cells .…”

Section: Exosomal Mirnas In Bc Drug Resistancecontrasting

confidence: 61%

Emerging roles of exosomal miRNAs in breast cancer drug resistance

Najminejad

Kalantar

Abdollahpour‐Alitappeh³

et al. 2019

IUBMB Life

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Breast cancer (BC), as a heterogeneous disease, is considered as one of the most common malignancies in women worldwide. The resistance of BC cells to therapeutic agents has remained a big challenge in the treatment of BC patients. Some factors such as cytokines, exosomes, and soluble receptors were recognized as crucial agents involved in the development of drug resistance. However, the exact mechanisms underlying the drug resistance is still unknown. There is growing evidence to support the emerging roles of exosomes, especially exosomal miRNAs, in tumor initiation, angiogenesis, proliferation, migration, invasion, metastasis, and drug resistance. Therefore, identification of BC-specific exosomal miRNAs and their underlying mechanisms would be helpful to define sensitivity to therapeutic drugs and establish an appropriate therapeutic strategy. This review focuses mainly on the roles of exosomal miRNAs and their associated mechanisms in the resistance of BC cells to therapeutic agents, as well as critically examines the potential of these macromolecules as a treatment biomarker in BC patients. K E Y W O R D Sbreast cancer, exosomes, drug resistance, therapeutics, exosomal miRNA, microRNA 1 | INTRODUCTION Breast cancer (BC), after skin cancer, was reported to be the most common malignancy in women worldwide. 1 Conversely, BC was showed to have a low incidence rate in men, approximately 1%. BC does not kill in primary stage. It was shown that the 5-year survival rates are 99%, 84%, and 23% for women with localized BC, regional stage, and

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Section: Exosomal Mirnas In Bc Drug Resistancecontrasting

confidence: 61%

Emerging roles of exosomal miRNAs in breast cancer drug resistance

Najminejad

Kalantar

Abdollahpour‐Alitappeh³

et al. 2019

IUBMB Life

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“…One of the miRs we found upregulated in MCF-7, miR-424, was also shown to be induced by 17-β-estradiol in at least two (95,96) of the multiple studies conducted in MCF-7. In some cases, ethanol induced upregulation is also seen after estrogen treatment, such as in miR-27a and b (96).…”

Section: Discussionmentioning

confidence: 61%

“…In some cases, ethanol induced upregulation is also seen after estrogen treatment, such as in miR-27a and b (96). The fact that ethanol affected any particular miR in this study did not necessarily coincide with affects on other miRs that would be expected to change comcomitantly if ethanol action were limited to one specific pathway such as the estrogenic pathway: thus upregulated miRs such as miR-107, miR-424, miR-570, miR-618, and miR-760 (95), miR-21 (28), miR-34b (97), miR-98 (98), miR-19A and miR-24 (96), miR-26a and b (99), miR-17 (100,101), miR-7 (102), or miR-190a (103); or downregulated miRs such as miR-16, miR-143, or miR-203 (104). Interestingly, the latter is the opposite of what we observed with ethanol.…”

Section: Discussionmentioning

confidence: 99%

Long-term exposure of MCF-7 breast cancer cells to ethanol stimulates oncogenic features

Gelfand

Vernet

Bruhn

et al. 2016

International Journal of Oncology

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Alcohol consumption is a risk factor for breast cancer. Little is known regarding the mechanism, although it is assumed that acetaldehyde or estrogen mediated pathways play a role. We previously showed that long-term exposure to 2.5 mM ethanol (blood alcohol ~0.012%) of MCF-12A, a human normal epithelial breast cell line, induced epithelial mesenchymal transition (EMT) and oncogenic transformation. In this study, we investigated in the human breast cancer cell line MCF-7, whether a similar exposure to ethanol at concentrations ranging up to peak blood levels in heavy drinkers would increase malignant progression. Short-term (1-week) incubation to ethanol at as low as 1–5 mM (corresponding to blood alcohol concentration of ~0.0048–0.024%) upregulated the stem cell related proteins Oct4 and Nanog, but they were reduced after exposure at 25 mM. Long-term (4-week) exposure to 25 mM ethanol upregulated the Oct4 and Nanog proteins, as well as the malignancy marker Ceacam6. DNA microarray analysis in cells exposed for 1 week showed upregulated expression of metallothionein genes, particularly MT1X. Long-term exposure upregulated expression of some malignancy related genes (STEAP4, SERPINA3, SAMD9, GDF15, KRT15, ITGB6, TP63, and PGR, as well as the CEACAM, interferon related, and HLA gene families). Some of these findings were validated by RT-PCR. A similar treatment also modulated numerous microRNAs (miRs) including one regulator of Oct4 as well as miRs involved in oncogenesis and/or malignancy, with only a few estrogen-induced miRs. Long-term 25 mM ethanol also induced a 5.6-fold upregulation of anchorage-independent growth, an indicator of malignant-like features. Exposure to acetaldehyde resulted in little or no effect comparable to that of ethanol. The previously shown alcohol induction of oncogenic transformation of normal breast cells is now complemented by the current results suggesting alcohol's potential involvement in malignant progression of breast cancer.

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“…The expression of several hemostatic factors has been reported to be regulated by miRNAs [23,24] including key procoagulant factors and inhibitors of the coagulation pathway as well as plasminogen activator inhibitor-1, the main modulator of fibrinolysis [25][26][27][28][29][30][31][32][33][34][35][36][37] (Table 1 and Figure 1). In a recent study, Nourse et al (2018) [38] revealed that individual genes encoding key hemostatic factors can be targeted by multiple miRNAs, suggesting that miRNAs act cooperatively in the regulation of the hemostatic system.…”

Section: Introductionmentioning

confidence: 99%

Role of microRNAs in Venous Thromboembolism

Morelli

Brækkan

Hansen

2020

IJMS

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MicroRNAs (miRNAs) are non-coding RNAs that execute their function by targeted downregulation of gene expressions. There is growing evidence from epidemiological studies and animal models suggesting that the expression level of miRNAs is dysregulated in venous thromboembolism (VTE). In this review, we summarize the current knowledge on the role of miRNAs as biomarkers for VTE and provide general insight into research exploring the modulation of miRNA activity in animal models of venous thrombosis. Up to now, published studies have yielded inconsistent results on the role of miRNAs as biomarkers for VTE with most of the reports focused on diagnostic research. The limited statistical power of the individual studies, due to the small sample sizes, may substantially contribute to the poor reproducibility among studies. In animal models, over-expression or inhibition of some miRNAs appear to influence venous thrombus formation and resolution. However, there is an important gap in knowledge on the potential role of miRNAs as therapeutic targets in VTE. Future research involving large cohorts should be designed to clarify the clinical usefulness of miRNAs as biomarkers for VTE, and animal model studies should be pursued to unravel the role of miRNAs in the pathogenesis of VTE and their potential as therapeutic targets.

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

Cited by 32 publications

References 51 publications

Emerging roles of exosomal miRNAs in breast cancer drug resistance

Emerging roles of exosomal miRNAs in breast cancer drug resistance

Long-term exposure of MCF-7 breast cancer cells to ethanol stimulates oncogenic features

Role of microRNAs in Venous Thromboembolism

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