mi<scp>RNA</scp>‐30e regulates abnormal differentiation of small intestinal epithelial cells in diabetic mice by downregulating Dll4 expression

Shan, Ti‐Dong; Ouyang, Hui; Yu, Tao; Li, Jieyao; Huang, Cuiqing; Yang, Hongsheng; Wu, Zhong; Xia, Zhen; Chen, Qi‐Kui

doi:10.1111/cpr.12230

Cited by 34 publications

(37 citation statements)

References 43 publications

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“…MicroRNAs (miRNAs) are a group of small, nonprotein coding, endogenous and single-stranded RNAs that negatively regulate target mRNA to either translational or mRNA degradation (7)(8)(9)(10)(11)(12). Emerging evidence has shown that miRNAs play pivotal roles in cellular functions, such as apoptosis, proliferation, motility and differentiation (13)(14)(15)(16)(17). Aberrant miRNA expression is found in various cancers including gastric, breast cancer, glioma, hepatocellular carcinoma, ovarian carcinoma, osteosarcoma and PDAC (7,(18)(19)(20)(21)(22)(23).…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-448 suppresses metastasis of pancreatic ductal adenocarcinoma through targeting JAK1/STAT3 pathway

Zhang

Wu³

et al. 2017

Oncology Reports

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Pancreatic ductal adenocarcinoma (PDAC) is the most common type of malignant pancreatic tumor. MicroRNAs (miRNAs) are a group of small, non-protein coding, endogenous RNAs that play critical roles in tumorigenesis and progression of PDAC. In the present study, we demonstrated that miR-448 expression was downregulated in PDAC tissues and cell lines. Clinical association analysis indicated that low expression of miR-448 was associated with poor prognostic features and conferred a significant reduced survival of PDAC patients. Overexpression of miR-448 suppressed PDAC cell migration and invasion, while its loss showed the opposite effects on these cellular processes. In vivo experiments revealed that miR-488 restoration prohibited liver metastasis of PDAC in nude mice. Moreover, we found that Janus kinase 1 (JAK1) was a direct target gene of miR-448 in PDAC cells. We further demonstrated that the expression of JAK1 mRNA was upregulated in PDAC tissues. Notably, the expression of JAK1 mRNA was inversely correlated with the level of miR-448 in PDAC tissues. In addition, JAK1 knockdown showed similar effects of miR-448 on the metastasis of PDAC cells. JAK1/STAT3 pathway may be involved in the function of miR-448 in PDAC cells. Taken together, these findings suggest that miR-448 functions as a tumor suppressor in the development of PDAC through targeting the JAK1/STAT3 pathway.

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Section: Introductionmentioning

confidence: 99%

MicroRNA-448 suppresses metastasis of pancreatic ductal adenocarcinoma through targeting JAK1/STAT3 pathway

Zhang

Wu³

et al. 2017

Oncology Reports

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“…The Notch signaling pathway is a highly conserved signaling mechanism in many processes determining cell fate during development in the adult organism . Activation of Notch occurs following Notch receptor/ligand engagement, which initiates translocation of the Notch intracellular domain to the nucleus and activation of target genes .…”

Section: Resultsmentioning

confidence: 99%

Tetrahedral DNA Nanostructure: A Potential Promoter for Cartilage Tissue Regeneration via Regulating Chondrocyte Phenotype and Proliferation

Shao

Lin

Peng

et al. 2017

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Utilizing biomaterials to regulate the phenotype and proliferation of chondrocytes is a promising approach for effective cartilage tissue regeneration. Recently, a significant amount of effort has been invested into directing chondrocytes toward a desired location and function by utilizing biomaterials to control the dedifferentiation and phenotypic loss of chondrocytes during in vitro monolayer culture. Here, the transmission signals resulting from tetrahedral DNA nanostructures (TDNs) in the regulation of chondrocyte phenotype and proliferation are exploited. TDNs, new DNA nanomaterials, have been considered as promising materials in biomedical fields. Upon exposure to TDNs, chondrocyte phenotype is significantly enhanced, accompanied by lower gene expression related to Notch signaling pathway and higher expression of type II collagen. In addition, the cell proliferation and morphology of chondrocytes are changed after exposure to TDNs. In conclusion, this work demonstrates that TDNs are potentially useful mechanism in cartilage tissue regeneration from chondrocytes, whereby chondrocyte phenotype and proliferation can be retained.

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“…When we looked at potential target molecules for miR-30, we found through in silico analyses that it may target the 3’UTR of Dll4 ( Supplemental Figures 2A–2C ) Previous studies had confirmed miR-30- Dll4 targeting using luciferase reporter assay 30 , 31 . Interestingly, DLL4 has been shown to be involved in Notch signaling 9 , 32 , 33 .…”

Section: Resultsmentioning

confidence: 99%

MicroRNA-30 modulates metabolic inflammation by regulating Notch signaling in adipose tissue macrophages

et al. 2018

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Background/Objectives Obesity is a pandemic disorder that is characterized by accumulation of adipose tissue and chronic-low grade inflammation that is driven primarily by adipose tissue macrophages (ATMs). While ATM polarization from pro-(M1)to anti-(M2) inflammatory phenotype influences insulin sensitivity and energy expenditure, the mechanisms of such a switch are unclear. In the current study we identified epigenetic pathways including microRNAs (miR) in ATMs that regulate obesity-induced inflammation. Subjects/Methods Male C57BL/6J mice were fed normal chow diet (NCD) or high-fat diet (HFD) for 16 weeks to develop lean and diet-induced obese mice respectively. Transcriptome microarrays, microRNA microarrays, and meDIP-Seq were performed on ATMs isolated from visceral fat. Pathway analysis and bone marrow derived macrophage (BMDM) transfections further allowed computational and functional analysis of miRNA-mediated ATM polarization. Results ATMs from HFD-fed mice were skewed towards M1 inflammatory phenotype. Concurrently, the expression of miRs 30a-5p, 30c-5p, and 30e-5p was downregulated in ATMs from HFD mice when compared to mice fed NCD. The miR-30 family was shown to target Delta-like-4, a Notch1 ligand, whose expression was increased in HFD ATMs. Inhibition of miR-30 in conditioned BMDM triggered Notch1 signaling, pro-inflammatory cytokine production, and M1 macrophage polarization. In addition, DNA hypermethylation was observed in mir30-associated CpG islands suggesting HFD downregulates miR-30 through epigenetic modifications. Conclusions HFD-induced obesity downregulates miR-30 by DNA methylation thereby inducing Notch1 signaling in ATMs and their polarization to M1 macrophages. These findings identify miR-30 as a regulator of pro-inflammatory ATM polarization and suggest miR-30 manipulation could be a therapeutic target for obesity-induced inflammation.

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miRNA‐30e regulates abnormal differentiation of small intestinal epithelial cells in diabetic mice by downregulating Dll4 expression

Abstract: Increased levels of miRNA-30e downregulated activity of the Dll4/NICD/Hes1 signalling pathway by targeting the 3'-UTR of Dll4, which contributed to abnormal differentiation in small intestinal epithelia of DM mice.

Cited by 34 publications

References 43 publications

MicroRNA-448 suppresses metastasis of pancreatic ductal adenocarcinoma through targeting JAK1/STAT3 pathway

MicroRNA-448 suppresses metastasis of pancreatic ductal adenocarcinoma through targeting JAK1/STAT3 pathway

Tetrahedral DNA Nanostructure: A Potential Promoter for Cartilage Tissue Regeneration via Regulating Chondrocyte Phenotype and Proliferation

MicroRNA-30 modulates metabolic inflammation by regulating Notch signaling in adipose tissue macrophages

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