Fibulin-5 promotes airway smooth muscle cell proliferation and migration via modulating Hippo-YAP/TAZ pathway

Fu, Jia; Zheng, Mao; Zhang, Xiaofang; Zhang, Yufeng; Chen, Yao; Li, Hua; Wang, Xiaowei; Zhang, Jinjun

doi:10.1016/j.bbrc.2017.09.105

Cited by 25 publications

(35 citation statements)

References 32 publications

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“…Integrins and integrin-ECM adhesion play important roles in cancer progression and metastasis [ 269 , 270 , 271 , 272 , 273 , 274 ], and integrin signaling is activated in many cancers [ 275 , 276 ]. A fair amount of evidence showing that integrin-ECM adhesion promotes YAP/TAZ activity has emerged [ 244 , 245 , 247 , 248 , 250 , 251 , 262 , 277 , 278 , 279 , 280 , 281 , 282 , 283 , 284 , 285 , 286 , 287 ]. Several of these studies show that knockdown or inhibition of all β1 integrins can reduce YAP/TAZ activity in a variety of cell types [ 245 , 247 , 277 , 278 , 279 , 280 ].…”

Section: Therapeutic Potential Of Targeting Yap/taz-tead In Cancermentioning

confidence: 99%

“…A fair amount of evidence showing that integrin-ECM adhesion promotes YAP/TAZ activity has emerged [ 244 , 245 , 247 , 248 , 250 , 251 , 262 , 277 , 278 , 279 , 280 , 281 , 282 , 283 , 284 , 285 , 286 , 287 ]. Several of these studies show that knockdown or inhibition of all β1 integrins can reduce YAP/TAZ activity in a variety of cell types [ 245 , 247 , 277 , 278 , 279 , 280 ]. However, these studies did not identify which of the 12 unique β1 integrins were involved, but instead suggested that integrin-mediated adhesion and spreading are generally important for YAP/TAZ activity.…”

Section: Therapeutic Potential Of Targeting Yap/taz-tead In Cancermentioning

confidence: 99%

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YAP/TAZ Activation as a Target for Treating Metastatic Cancer

Warren

Xiao

2018

Cancers

142

131

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Yes-Associated Protein (YAP) and Transcriptional Co-activator with PDZ-binding Motif (TAZ) have both emerged as important drivers of cancer progression and metastasis. YAP and TAZ are often upregulated or nuclear localized in aggressive human cancers. There is abundant experimental evidence demonstrating that YAP or TAZ activation promotes cancer formation, tumor progression, and metastasis. In this review we summarize the evidence linking YAP/TAZ activation to metastasis, and discuss the roles of YAP and TAZ during each step of the metastatic cascade. Collectively, this evidence strongly suggests that inappropriate YAP or TAZ activity plays a causal role in cancer, and that targeting aberrant YAP/TAZ activation is a promising strategy for the treatment of metastatic disease. To this end, we also discuss several potential strategies for inhibiting YAP/TAZ activation in cancer and the challenges each strategy poses.

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Section: Therapeutic Potential Of Targeting Yap/taz-tead In Cancermentioning

confidence: 99%

Section: Therapeutic Potential Of Targeting Yap/taz-tead In Cancermentioning

confidence: 99%

YAP/TAZ Activation as a Target for Treating Metastatic Cancer

Warren

Xiao

2018

Cancers

142

131

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“…1C and Table 3, the 2 most related transcription factors were identi ed to be NOTCH1 and YAP1. The YAP1 factor has been widely correlated with asthma [21,22], and can also in uence disease progression by mediating HIF-1α in both liver cancer and pancreatic cancer [10,23]. Meanwhile [24], NOTCH1 is involved in the promotion of the GATA3-mediated Th2 response (immunity), which makes NOTCH1 an unlikely candidate responsible for the non-Th2 in ammatory pattern in asthma.…”

Section: Resultsmentioning

confidence: 99%

The YAP/HIF-1α/miR-182/EGR2 Axis is Implicated in Asthma Severity by Control of Th17 Cell Differentiation

Zhou

Zhang

et al. 2020

Preprint

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Background: Asthma is a heterogeneous chronic inflammatory disease of the airways, with reversible airflow limitations and airway remodeling. T helper 17 (Th17) cells play an important role in the pathogenesis of allergic asthma. However, there is hitherto little data about signaling pathways controlling Th17 cell differentiation in asthma. The aim of this study was to ascertain whether the YAP/HIF-1α/miR-182/EGR2 axis underpins Th17 cell differentiation and asthma severity.Methods: The study included 29 pediatric patients with asthma, 22 healthy volunteers, ovalbumin (OVA)-induced murine asthma models, and mouse naive CD4+ T. The subpopulation of Th17 cells was examined by flow cytometry. The level of IL-17A was determined by ELISA method. ChIP-qPCR assay and dual-luciferase reporter gene assay were performed to examine interaction between HIF-1α and miR-182, miR-182 and EGR2.Results: YAP, HIF-1α, and miR-182 were found to be up-regulated but EGR2 was down-regulated in human and mouse peripheral blood mononuclear cells (PBMCs) in the context of asthma. Abundant expression of YAP and HIF-1α promoted miR-182 expression and then inhibited EGR2, a target of miR-182, thus enhancing Th17 differentiation and deteriorating asthma and lipid metabolism dysfunction. In addition, in vivo findings revealed that over-expression of EGR2 undermined the promoting effect of the YAP/HIF-1α/miR-182 axis on asthma and lipid metabolism dysfunction.Conclusion: These results shed light on that the activation of the YAP/HIF-1α/miR-182/EGR2 axis may promote Th17 cell differentiation, exacerbate asthma development, and aggravate lipid metabolism dysfunction, providing a potential therapeutic target in asthma.

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“…Knockdown of YAP1 induces cellular senescence [30] and suppresses angiogenesis and organ regeneration (e.g., liver) in aged adults [31]. Deregulation of YAP1 signaling also contributes to aging-associated diseases such as COPD [32], pulmonary fibrosis [18, 33], and Alzheimer’s disease [34, 35]. Rho-GTPase CDC42 senses mechanical forces, induces filopodia formation and regulates cellular adhesions and polarity in various types of cells including ECs and fibroblasts [36, 37].…”

Section: Introductionmentioning

confidence: 99%

Effects of age-dependent changes in cell size on endothelial cell proliferation and senescence through YAP1

Mammoto

Torisawa

Muyleart

et al. 2019

Aging

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Angiogenesis – the growth of new blood capillaries- is impaired in aging animals. Biophysical factors such as changes in cell size control endothelial cell (EC) proliferation and differentiation. However, the effects of aging on EC size and the mechanism by which changes in cell size control age-dependent decline in EC proliferation are largely unknown. Here, we have demonstrated that aged ECs are larger than young ECs and that age-dependent increases in EC size control EC proliferation and senescence through CDC42-Yes-associated protein (YAP1) signaling. Reduction of aged EC size by culturing on single-cell sized fibronectin-coated smaller islands decreases CDC42 activity, stimulates YAP1 nuclear translocation and attenuates EC senescence. Stimulation of YAP1 or inhibition of CDC42 activity in aged ECs also restores blood vessel formation. Age-dependent changes in EC size and/or CDC42 and YAP1 activity may be the key control point of age-related decline in angiogenesis.

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Fibulin-5 promotes airway smooth muscle cell proliferation and migration via modulating Hippo-YAP/TAZ pathway

Cited by 25 publications

References 32 publications

YAP/TAZ Activation as a Target for Treating Metastatic Cancer

YAP/TAZ Activation as a Target for Treating Metastatic Cancer

The YAP/HIF-1α/miR-182/EGR2 Axis is Implicated in Asthma Severity by Control of Th17 Cell Differentiation

Effects of age-dependent changes in cell size on endothelial cell proliferation and senescence through YAP1

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