Noncoding RNAs and the control of hormonal signaling via nuclear receptor regulation

Ottaviani, Silvia; Giorgio, Alex de; Harding, Victoria; Stebbing, Justin; Castellano, Leandro

doi:10.1530/jme-14-0134

Cited by 11 publications

(5 citation statements)

References 103 publications

(104 reference statements)

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“…On the other hand, Drosha is responsible for the cleavage of pri-miRNAs into pre-miRNAs, and then further processed by Dicer to produce mature miR-33a (Krol et al, 2010 ). Direct interaction of PPAR-γ with Drosha may thus decrease mature miR-33a biogenesis (Ottaviani et al, 2014 ).…”

Section: Discussionmentioning

confidence: 99%

Ginsenoside-Rb1-Mediated Anti-angiogenesis via Regulating PEDF and miR-33a through the Activation of PPAR-γ Pathway

Zhou

Kwok

et al. 2017

Front. Pharmacol.

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Angiogenesis is the formation of new blood vessels from the existing vasculature, which is involved in multiple biological processes, including atherosclerosis, ischemic heart disease, and cancer. Ginsenoside-Rb1 (Rb1), the most abundant ginsenoside isolated form Panax ginseng, has been identified as a promising anti-angiogenic agent via the up-regulation of PEDF. However, the underlying molecular mechanisms still unknown. In the present study, human umbilical vein endothelial cells (HUVECs) were selected to perform in vitro assays. Rb1 (0–20 nM) treatment induced pigment epithelial-derived factor (PEDF) protein expression in concentration and time-dependent manners. Interestingly, it was also demonstrated that the exposure of Rb1 (10 nM) could increase PEDF protein expression without any alteration on mRNA level, suggesting the involvement of posttranscriptional regulation. Furthermore, bioinformatics predictions indicated the regulation of miR-33a on PEDF mRNA 3′-UTR, which was further confirmed by luciferase reporter gene assay and real-time PCR. Over-expression of pre-miR-33a was found to regress partly Rb1-mediated PEDF increment and anti-angiogenic effect in HUVECs. Additionally, Rb1-reduced miR-33a and increased PEDF expression was prevented by pre-incubation with peroxisome proliferator-activated receptor-γ (PPAR-γ) antagonist (GW9662) or transfection with PPAR-γ siRNA in HUVECs. Taken together, our findings demonstrated that Rb1 exerted anti-angiogenic effects through PPAR-γ signaling pathway via modulating miR-33a and PEDF expressions. Thus, Rb1 may have the potential of being developed as an anti-angiogenic agent, however, further appropriate studies are warranted to evaluate the effect in vivo.

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Section: Discussionmentioning

confidence: 99%

Ginsenoside-Rb1-Mediated Anti-angiogenesis via Regulating PEDF and miR-33a through the Activation of PPAR-γ Pathway

Zhou

Kwok

et al. 2017

Front. Pharmacol.

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“…Hormone receptors could be interconnected with lncRNAs expression in the cells and this relation could affect cellular metabolism (37). Moreover, in SNHG6 203 overexpression situation, the complicated behavior of MCF7 and SK-BR3 cells could be attributed to different hormonal signaling (38,39). Overall, the results of this study demonstrated an interconnection between SNHG6 203 RNA and HER2 status of breast tumoral cells that might indicate SNHG6 203 probable role in the cell cycle progression of HER2-negative breast cancers.…”

Section: Discussionmentioning

confidence: 66%

SNHG6 203 RNA May be Involved in the Cell Cycle Progression in HER2-Negative Breast Cancer Cells

Oliayi

Dabiri

2022

Iran J Pathol

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Scan to discover onlineBackground & Objective: Long noncoding RNAs (lncRNAs) as challenging molecules are more known than those in the last decade. These transcripts have been validated for carcinogenesis in many types of tissue. Functions of lncRNAs in cancer induction include cell cycle, epithelial to mesenchymal transition progression, apoptosis inhibition, cell migration, and invasion stimulation. LncRNA small nucleolar host gene 6 (SNHG6) have been proven as an oncogenic transcript in many types of cancer.Methods: RNA extraction was performed for 47 breast specimens in patients with cancer and cDNAs were synthesized. Relative expression of target variants was determined by qPCR and calculated based on the ΔΔCt method. SNHG6 203 was cloned into pcDNA 3.1+ vector for overexpression in MCF7 (HER2-) and SK-BR3 (HER2+) cells. The cell cycle progression of transfected cells was assessed by flow cytometry. Cell migration ability of transfected cells was evaluated by the scratch method and Image J software. Finally, cell viability was assessed by the MTT method.Results: Among four splice variants of SNHG6 (202, 203, 204, and 207), SNHG6 203 was proved as an overexpressed splice variant in breast tumors. This transcript was expressed in HER2-negative breast tumors more frequently than in the positive ones. Overexpression of this variant in target cells resulted in cell cycle progression of MCF7 as HER2-negative cells. Moreover, the overexpression of SNHG6 203 led to lower migration ability of MCF7 cells and a non-significant reduction of their viability as HER2-negative breast cancer cells. Conclusion:Our results revealed that SNHG6 203 may be involved in the carcinogenesis of HER2-negative breast cancers via cell cycle progression.

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“…Recently RARα was identified to regulate protein synthesis to some extent by its binding to a subset of mRNAs in human platelets 43 . Hence, it is possible that other NRs including PXR (in a bound or unbound state with RXR) may also contribute to some level of protein translation even in the absence of a nucleus 44,45 . To date, we have found no evidence to indicate the formation of NR homodimers in platelets.…”

Section: Discussionmentioning

confidence: 99%

Non-genomic effects of the Pregnane X Receptor negatively regulate platelet functions, thrombosis and haemostasis

Flora

Sahli

Sasikumar

et al. 2019

Sci Rep

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The pregnane X receptor (PXR) is a nuclear receptor (NR), involved in the detoxification of xenobiotic compounds. Recently, its presence was reported in the human vasculature and its ligands were proposed to exhibit anti-atherosclerotic effects. Since platelets contribute towards the development of atherosclerosis and possess numerous NRs, we investigated the expression of PXR in platelets along with the ability of its ligands to modulate platelet activation. The expression of PXR in human platelets was confirmed using immunoprecipitation analysis. Treatment with PXR ligands was found to inhibit platelet functions stimulated by a range of agonists, with platelet aggregation, granule secretion, adhesion and spreading on fibrinogen all attenuated along with a reduction in thrombus formation (both in vitro and in vivo). The effects of PXR ligands were observed in a species-specific manner, and the human-specific ligand, SR12813, was observed to attenuate thrombus formation in vivo in humanised PXR transgenic mice. PXR ligand-mediated inhibition of platelet function was found to be associated with the inhibition of Src-family kinases (SFKs). This study identifies acute, non-genomic regulatory effects of PXR ligands on platelet function and thrombus formation. In combination with the emerging anti-atherosclerotic properties of PXR ligands, these anti-thrombotic effects may provide additional cardio-protective benefits.

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Noncoding RNAs and the control of hormonal signaling via nuclear receptor regulation

Cited by 11 publications

References 103 publications

Ginsenoside-Rb1-Mediated Anti-angiogenesis via Regulating PEDF and miR-33a through the Activation of PPAR-γ Pathway

Ginsenoside-Rb1-Mediated Anti-angiogenesis via Regulating PEDF and miR-33a through the Activation of PPAR-γ Pathway

SNHG6 203 RNA May be Involved in the Cell Cycle Progression in HER2-Negative Breast Cancer Cells

Non-genomic effects of the Pregnane X Receptor negatively regulate platelet functions, thrombosis and haemostasis

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