MicroRNA‐155 is a novel suppressor of ovarian cancer‐initiating cells that targets CLDN1

Qin, Wenxing; Ren, Qiusheng; Liu, Te; Huang, Yongyi; Wang, Jiejun

doi:10.1016/j.febslet.2013.03.023

Cited by 114 publications

(77 citation statements)

References 23 publications

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“…CLDN1, one of the major components of TJs, is among the direct targets of miR‐155 42, 43. While CLDN5 is highly expressed in the brain endothelium, CLDN1 expression in cerebral capillaries is low and was only confirmed to be present in human, rat, and sheep BBB 3, 30, 31.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of MicroRNA‐155 Supports Endothelial Tight Junction Integrity Following Oxygen‐Glucose Deprivation

Peña-Philippides

Gardiner

Caballero-Garrido

et al. 2018

JAHA

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BackgroundBrain microvascular endothelial cells form a highly selective blood brain barrier regulated by the endothelial tight junctions. Cerebral ischemia selectively targets tight junction protein complexes, which leads to significant damage to cerebral microvasculature. Short noncoding molecules called microRNAs are implicated in the regulation of various pathological states, including endothelial barrier dysfunction. In the present study, we investigated the influence of microRNA‐155 (miR‐155) on the barrier characteristics of human primary brain microvascular endothelial cells (HBMECs).Methods and ResultsOxygen‐glucose deprivation was used as an in vitro model of ischemic stroke. HBMECs were subjected to 3 hours of oxygen‐glucose deprivation, followed by transfections with miR‐155 inhibitor, mimic, or appropriate control oligonucleotides. Intact normoxia control HBMECs and 4 oxygen‐glucose deprivation–treated groups of cells transfected with appropriate nucleotide were subjected to endothelial monolayer electrical resistance and permeability assays, cell viability assay, assessment of NO and human cytokine/chemokine release, immunofluorescence microscopy, Western blot, and polymerase chain reaction analyses. Assessment of endothelial resistance and permeability demonstrated that miR‐155 inhibition improved HBMECs monolayer integrity. In addition, miR‐155 inhibition significantly increased the levels of major tight junction proteins claudin‐1 and zonula occludens protein‐1, while its overexpression reduced these levels. Immunoprecipitation and colocalization analyses detected that miR‐155 inhibition supported the association between zonula occludens protein‐1 and claudin‐1 and their stabilization at the HBMEC membrane. Luciferase reporter assay verified that claudin‐1 is directly targeted by miR‐155.ConclusionsBased on these results, we conclude that miR‐155 inhibition–induced strengthening of endothelial tight junctions after oxygen‐glucose deprivation is mediated via its direct target protein claudin‐1.

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Section: Discussionmentioning

confidence: 99%

Inhibition of MicroRNA‐155 Supports Endothelial Tight Junction Integrity Following Oxygen‐Glucose Deprivation

Peña-Philippides

Gardiner

Caballero-Garrido

et al. 2018

JAHA

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“…According to the results in luciferase reporter assay, the miR-30c was related to the invasion of NSCLC by regulating MTA1. MiRNAs can regulate the target gene expression by binding its 3′-UTR [26,27,28]. However, the mechanism of miR-30c requires further research.…”

Section: Discussionmentioning

confidence: 99%

Down-Regulation of MiR-30c Promotes the Invasion of Non-Small Cell Lung Cancer by Targeting MTA1

Xia

Chen

Zhong

et al. 2013

Cell Physiol Biochem

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Background: The connection between microRNA expression and lung cancer development has been identified in recent literature. However, the mechanism of microRNA has been poorly elucidated in non-small-cell lung cancer (NSCLC). Methods and Results: Comparing with adjacent tissues (n=75), miR-30c has a lower expression in lung cancer specimens (n=75). The knockdown of miR-30c enhanced the invasion of A549 cells; meanwhile, the overexpression of miR-30c could reverse the effect of the knockdown of miR-30c in vitro. A luciferase assay revealed that miR-30c was directly bound to the 3‘-untranslated regions (3‘-UTR) of MTA1. QRT-PCR and western blot shows MTA1 was up-regulated in mRNA and protein levels. The effect taken on the invasion of NSCLC by overexpression of MTA1 works the same as down-regulated miR-30c. Conclusion: miR-30c may play a pivotal role in controlling lung cancer invasion through regulating MTA1in NSCLC.

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“…Recently, it was demonstrated that miR-155 is up-regulated by the transforming growth factor β (TGF-β) pathway, which plays an important role in TGF-β-induced EMT in breast cancer cells [25]. In addition, a recent study showed that miR-155 overexpression inhibits ovarian cancer-initiating cell proliferation and invasion [26]. However, the role of miR-155 in HCC cells during the EMT and acquisition of the cancer stem cell phenotype is not fully understood.…”

Section: Introductionmentioning

confidence: 99%

TGF-β1 acts through miR-155 to down-regulate TP53INP1 in promoting epithelial–mesenchymal transition and cancer stem cell phenotypes

Liu

Kong

et al. 2015

Cancer Letters

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MicroRNA‐155 is a novel suppressor of ovarian cancer‐initiating cells that targets CLDN1

Cited by 114 publications

References 23 publications

Inhibition of MicroRNA‐155 Supports Endothelial Tight Junction Integrity Following Oxygen‐Glucose Deprivation

Inhibition of MicroRNA‐155 Supports Endothelial Tight Junction Integrity Following Oxygen‐Glucose Deprivation

Down-Regulation of MiR-30c Promotes the Invasion of Non-Small Cell Lung Cancer by Targeting MTA1

TGF-β1 acts through miR-155 to down-regulate TP53INP1 in promoting epithelial–mesenchymal transition and cancer stem cell phenotypes

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