Matricellular Protein Cyr61 Bridges Lysophosphatidic Acid and Integrin Pathways Leading to Cell Migration

Wu, Daniel Dongwei; Zhang, Fuqiang; Feng, Hao; Chun, Jerold; Xu, Xuemin; Cui, Mei‐Zhen

doi:10.1074/jbc.m113.533042

Cited by 23 publications

(22 citation statements)

References 53 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…49 Interaction of Cyr61 with integrin increases FAK phosphorylation, which enhances AKT activation. 50 AKT has been a critical mediator of cell proliferation, survival and metastasis in a variety of cell types. 51 Results of the present study show that AMOT downregulation increases FAK and AKT phosphorylation, which are inhibited by Cyr61 silencing.…”

Section: Discussionmentioning

confidence: 99%

Angiomotin decreases lung cancer progression by sequestering oncogenic YAP/TAZ and decreasing Cyr61 expression

Hsu

et al. 2014

Oncogene

View full text Add to dashboard Cite

Lung cancer is the leading cause of cancer death worldwide, with metastasis underlying majority of related deaths. Angiomotin (AMOT), a scaffold protein, has been shown to interact with oncogenic Yes-associated protein/transcriptional co-activator with a PDZ-binding motif (YAP/TAZ) proteins, suggesting a potential role in tumor progression. However, the functional role of AMOT in lung cancer remains unknown. This study aimed to identify the patho-physiological characteristics of AMOT in lung cancer progression. Results revealed that AMOT expression was significantly decreased in clinical lung cancer specimens. Knockdown of AMOT in a low metastatic CL1-0 lung cancer cell line initiated cancer proliferation, migration, invasion and epithelial-mesenchymal transition. The trigger of cancer progression caused by AMOT loss was transduced by decreased cytoplasmic sequestration and increased nuclear translocation of oncogenic co-activators YAP/TAZ, leading to increased expression of the growth factor, Cyr61. Tumor promotion by AMOT knockdown was reversed when YAP/TAZ or Cyr61 was absent. Further, AMOT knockdown increased the growth and spread of Lewis lung carcinoma in vivo. These findings suggest that AMOT is a crucial suppressor of lung cancer metastasis and highlight its critical role as a tumor suppressor and its potential as a prognostic biomarker and therapeutic target for lung cancer.

show abstract

Section: Discussionmentioning

confidence: 99%

Angiomotin decreases lung cancer progression by sequestering oncogenic YAP/TAZ and decreasing Cyr61 expression

Hsu

et al. 2014

Oncogene

View full text Add to dashboard Cite

show abstract

“…Therefore, Cyr61 seems to be the long-missing, important extracellular mediator in the PDGF pathway. Our recent study has demonstrated that Cyr61 is a key mediator for lysophosphatidic acid-induced cell migration (51). One previous article showed that Cyr61 mediates thrombin-induced cell proliferation (52).…”

Section: Discussionmentioning

confidence: 99%

The Matricellular Protein Cyr61 Is a Key Mediator of Platelet-derived Growth Factor-induced Cell Migration

Zhang

Feng

et al. 2015

Journal of Biological Chemistry

Self Cite

View full text Add to dashboard Cite

Background: PDGF is a potent chemoattractant for cells. Results:The PDGF-induced extracellular matrix component Cyr61 bridges the intracellular PDGF-ERK and JNK signaling pathways with integrin/FAK signaling, leading to cell migration. Conclusion: Cyr61 is a key mediator of PDGF-induced cell migration via the Cyr61-integrin-FAK pathway. Significance: Extracellular Cyr61 convergence with growth factor and integrin/FAK signaling is a new cell migration concept.

show abstract

“…These same integrin/ECM signaling proteins can also influence YAP/TAZ regulation [20,43,146,151,152]. For example, in skeletal stem cells the membrane-anchored metalloproteinase MT1-MMP was found to activate the β1-integrin/RHO GTPase signaling cascade, which triggered the nuclear accumulation of YAP/TAZ and promoted skeletal stem cell lineage commitment [150].…”

Section: Yap/taz As a Signaling Networkmentioning

confidence: 99%

YAP and TAZ: a nexus for Hippo signaling and beyond

Hansen

Moroishi

Guan

2015

Trends in Cell Biology

472

482

View full text Add to dashboard Cite

The Hippo pathway is a potent regulator of cellular proliferation, differentiation, and tissue homeostasis. Here we review the regulatory mechanisms of the Hippo pathway and discuss the function of Yes-associated protein (YAP)/transcriptional coactivator with a PDZ-binding domain (TAZ), the prime mediators of the Hippo pathway, in stem cell biology and tissue regeneration. We highlight their activities in both the nucleus and the cytoplasm and discuss their role as a signaling nexus and integrator of several other prominent signaling pathways such as the Wnt, G protein-coupled receptor (GPCR), epidermal growth factor (EGF), BMP/transforming growth factor beta (TGFβ), and Notch pathways.

show abstract

Matricellular Protein Cyr61 Bridges Lysophosphatidic Acid and Integrin Pathways Leading to Cell Migration

Cited by 23 publications

References 53 publications

Angiomotin decreases lung cancer progression by sequestering oncogenic YAP/TAZ and decreasing Cyr61 expression

Angiomotin decreases lung cancer progression by sequestering oncogenic YAP/TAZ and decreasing Cyr61 expression

The Matricellular Protein Cyr61 Is a Key Mediator of Platelet-derived Growth Factor-induced Cell Migration

YAP and TAZ: a nexus for Hippo signaling and beyond

Contact Info

Product

Resources

About