MicroRNA-mRNA interactions controlled by TGF-b

Ottaviani, Silvia; Frampton, Adam; Chugh, Monika; Dama, Paola; Stiff, Thomas; Liu, Qi; Bayraktar, Salih; Krell, Jonathan; Magnani, Luca; Zagorac, Sladjana; Trabulo, Sara; Lemoine, Nicholas R.; Stebbing, Justin; Castellano, Leandro

doi:10.1016/j.pan.2020.10.010

Cited by 4 publications

(10 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In the present study, we integrated RIP-seq and RNA-seq data 17,21 of MIN6 cells transfected with control or miR-125 mimics which allowed us to identify dozens of miR-125b targets in an unbiased and high-throughput manner. One of the genes at the top of this list, M6pr, encodes the cation-dependent manose-6-phosphate protein MP6R (CD-M6PR).…”

Section: Discussionmentioning

confidence: 99%

“…Ottaviani and co-workers 17 have recently demonstrated that miR-125b is induced by TGF-β via Smad2/3 activation of the MIR125B-1 locus in pancreatic ductal adenocarcinoma cells (PDAC). Interestingly, Smad2/3 ChIP-seq in mouse islets showed binding to an annotated miR-125b TSS (Supp Figure 2) located in a chromatin region with increased accessibility in βLKB1KO islets (Cebola et al in preparation, Supp Fig 2).…”

Section: Glucose Stimulates Mir-125b Expression Via Ampk Repressionmentioning

confidence: 99%

“…MiRISC's action will result in target mRNA destabilization 20 and/or inhibition of target mRNA translation without observable changes in transcript levels. Thus, we used an experimental approach that combined overexpression of miR-125b in MIN6 cells, immunoprecipitation of miRISC/target mRNAs using an antibody against AGO2 and high-throughput sequencing and differential analysis of cellular total and immunoprecipitated RNAs 17,21 (Figure 3a). As a consequence of miR-125b overexpression, we expected miR-125b targets to be reduced or unchanged (if repression occurs exclusively at the level of translation) in the total mRNA (T-RNA, Sup Table 1) fraction and increased in the precipitated (RIP-RNA, Supp Table 1) fraction.…”

Section: High-through Identification Of Mir-125b Target Genesmentioning

confidence: 99%

“…MiRISC-immunoprecipitation was performed as previously described 17 and proteinase K (20mg/ml) (Thermo Fisher Scientific) for 20 min at room temperature. RNA was extracted using phenol/ chloroform and ethanol/sodium acetate precipitation.…”

Section: Mirisc Immunoprecipitationmentioning

confidence: 99%

See 3 more Smart Citations

Glucose-dependent miR-125b is a negative regulator of β-cell function

Cheung

Pizza

Chabosseau

et al. 2021

Preprint

View full text Add to dashboard Cite

Impaired pancreatic β-cell function and insulin secretion are hallmarks of type 2 diabetes. MicroRNAs are short non-coding RNAs that silence gene expression, vital for the development and function of endocrine cells. MiR-125b is a highly conserved miRNA abundant in β-cells, though its role in these cells remains unclear. Here, we show that miR-125b expression in human islets correlates with body mass index (BMI) of the donors and is regulated by glucose in an AMP-activated protein kinase-dependent manner in both mice and humans. Using and unbiased high-throughput approach, we identify dozens of direct gene targets, including the transporter of lysosomal hydrolases M6pr and the mitochondrial fission regulator Mtfp1. Whereas inactivation of miR-125b in human β-cells led to shorter mitochondria and improved glucose stimulated insulin secretion, mice over-expressing mir-125b selectively in β-cells displayed defective insulin secretion and marked glucose intolerance. Moreover, the β-cells of these transgenic animals showed strongly reduced insulin content and secretion and contained enlarged lysosomal structures. Thus, miR125b provides a glucose-controlled regulator of organelle dynamics that negatively regulates insulin secretion in β-cells.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Glucose Stimulates Mir-125b Expression Via Ampk Repressionmentioning

confidence: 99%

Section: High-through Identification Of Mir-125b Target Genesmentioning

confidence: 99%

Section: Mirisc Immunoprecipitationmentioning

confidence: 99%

See 2 more Smart Citations

Glucose-dependent miR-125b is a negative regulator of β-cell function

Cheung

Pizza

Chabosseau

et al. 2021

Preprint

View full text Add to dashboard Cite

show abstract

“…lncRNA-ATB induced liver cancer metastasis by upregulating the levels of zinc finger E-box-binding homeoboxes (ZEB) 1 and 2, which are involved in the induction of EMT [19]. In addition, lncRNA LIN28B was induced by TGF-β, which has been shown to promote the development and proliferation of pancreatic ductal adenocarcinoma [39]. The level of lncRNA-hDREH was decreased by hepatitis B virus X protein, which inhibits EMT in hepatocellular carcinoma (HCC) [40].…”

Section: Metastasismentioning

confidence: 99%

The Role of Sex-specific Long Non-coding RNAs in Cancer Prevention and Therapy

Song

Kim

2021

J Cancer Prev

View full text Add to dashboard Cite

The functions of a large number of non-coding genes in human DNA have yet to be accurately identified. Long non-coding RNA (lncRNA) measuring 10 kb or less in length regulates transcription or post-transcriptional events. The lncRNAs have attracted increased attention of researchers in recent years. In this review, we summarize the recently published lncRNAs which are known to influence cancer development and progression. We also discuss recent studies investigating tumor-specific lncRNA expression. These lncRNAs provide very useful information that allows prediction of the degree of malignancy and a survival rate in cancer patients as clinically relevant biomarkers. Because symptoms and progression of cancer differ from onset to death between males and females, it is important to consider the gender of the patient when diagnosing cancer and predicting the progression. Considering the importance of gender difference, we also examine the influence of sex hormones involved in the expression and regulation of lncRNAs as biomarkers. Many of the lncRNAs examined in this review have been studied in cancers occurring in the female or male reproductive organs, but the association between lncRNAs and sex hormones has also been reported in common organs such as the lung, renal and colon. Although lncRNAs have not yet been widely used as definitive cancer indicators, recent studies have demonstrated the potential role of lncRNAs as biomarkers and therapeutic targets reflecting sex-specificity in a number of different cancers.

show abstract

lncRNA NEAT1/miR‐495‐3p regulates angiogenesis in burn sepsis through the TGF‐β1 and SMAD signaling pathways

Meng

Hao

Zhang

et al. 2023

Immunity Inflam & Disease

View full text Add to dashboard Cite

Introduction:To investigate the role of the long-chain noncoding RNA (lncRNA) nuclear enriched abundant transcript 1 (NEAT1) in the process of angiogenesis in human umbilical vein endothelial cells (HUVECs) and illustrate its potential role in burn sepsis (BS) pathogenesis. Methods: HUVECs were treated with BS patient serum or healthy control serum.NEAT1 shRNA, miR-495-3p mimics, and miR-495-3p inhibitor were transfected into HUVECs. NEAT1 and miR-495-3 levels in serum or HUVECs were detected using quantitative reverse transcription-polymerase chain reaction. Cell counting kit-8 and flow cytometry assays were used to explore the proliferation and apoptosis of HUVECs. The expression of vascular endothelial growth factor (VEGF) in the supernatant was detected using enzyme-linked immunosorbent assay. Tube formation of HUVECs was also analyzed. Western blot analysis was used to analyze signaling pathway proteins.Results: In HUVECs stimulated with BS patient serum, NEAT1 expression was increased, while miR-495-3p expression was decreased. In addition, NEAT1 silencing by specific shRNA inhibited cell proliferation, VEGF production, and tube formation under burn patient serum treatment, which decreased the TGFβ1/SMAD signaling pathway activation. Moreover, miR-495-3p minics inhibited angiogenesis and the activation of signaling pathways induced by NEAT1 shRNA. Furthermore, miR-495-3p inhobitor promoted angiogenesis in HUVECs and activated the TGFβ1/SMAD signaling pathway. In patients with BS, NEAT1 expression was significantly increased and miR-495-3p expression was decreased compared to healthy controls, and NEAT1 and miR-495-3p expression was associated with the clinical features of patients. Conclusions:Our results indicate that lncRNA NEAT1 regulates angiogenesis and activates the TGFβ1/SMAD signaling pathway during the occurrence of BS.

show abstract

MicroRNA-mRNA interactions controlled by TGF-b

Cited by 4 publications

References 0 publications

Glucose-dependent miR-125b is a negative regulator of β-cell function

Glucose-dependent miR-125b is a negative regulator of β-cell function

The Role of Sex-specific Long Non-coding RNAs in Cancer Prevention and Therapy

lncRNA NEAT1/miR‐495‐3p regulates angiogenesis in burn sepsis through the TGF‐β1 and SMAD signaling pathways

Contact Info

Product

Resources

About