Vascular Endothelial Growth Factor (VEGF) Promotes Assembly of the p130Cas Interactome to Drive Endothelial Chemotactic Signaling and Angiogenesis

Evans, Ivor H.; Kennedy, Susan; Paliashvili, Ketevan; Santra, Tapesh; Yamaji, Maiko; Lovering, Ruth C.; Britton, Gary; Frankel, Paul; Kölch, Walter; Zachary, Ian

doi:10.1074/mcp.m116.064428

Cited by 28 publications

(21 citation statements)

References 52 publications

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“…Moreover, IQGAP1 can rapidly bind to VEGFR2 in endothelial cells under VEGF stimulation . Furthermore, the downregulation of IIQGAP1 expression can attenuate the migratory and proliferative abilities of VEGF‐induced endothelial cells . In addition, IQGAP1 −/− mice show markedly reduced VEGF expression in ischemic tissue contrasted with wild‐type mice .…”

Section: Discussionmentioning

confidence: 99%

Downregulation of IQGAP1 inhibits epithelial‐mesenchymal transition via the HIF1α/VEGF‐A signaling pathway in gastric cancer

Liu

et al. 2019

J of Cellular Biochemistry

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As an oncogene, IQ‐domain GTPase‐activating protein 1 (IQGAP1) regulates the epithelial‐mesenchymal transition (EMT) of several cancers, such as breast cancer, thyroid cancer, and esophageal squamous cell carcinoma. However, the role of the scaffold protein IQGAP1 on EMT in gastric cancer remains unclear. Therefore, the present work was performed to address the question. Our results showed that IQGAP1 expression is upregulated in human gastric cancer specimens and cell lines. Furthermore, IQGAP1 knockdown inhibited the migratory ability of gastric cancer cells and reduced the expression of mesenchymal phenotype markers, including Slug, β‐catenin, Snail, Vimentin, and N‐cadherin, as well as vascular endothelial growth factor‐A (VEGF‐A) secretion in gastric cancer cells. Conversely, IQGAP1 downregulation increased the epithelial phenotype marker E‐cadherin. Furthermore, IQGAP1 silencing not only downregulated hypoxia‐inducible transcription factor 1α (HIF1α) but also limited its translocation from the cytosol to the nucleus. Collectively, our results indicated that EMT was regulated by IQGAP1, which was associated with VEGF‐A, since other data demonstrated that HIF1α was involved in VEGF‐A expression. Therefore, we speculated that IQGAP1 regulated EMT of gastric cancer partially via the HIF1α/VEGF‐A signaling pathway. IQGAP1 may serve as an effective therapeutic biomarker for gastric cancer.

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Section: Discussionmentioning

confidence: 99%

Downregulation of IQGAP1 inhibits epithelial‐mesenchymal transition via the HIF1α/VEGF‐A signaling pathway in gastric cancer

Liu

et al. 2019

J of Cellular Biochemistry

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“…Providers of bioinformatics tools, such as g:Profiler (21), Cytoscape (22), or DAVID (23), import GO data into their tools for use in enrichment analyses of large datasets. Therefore, the association of GO terms with gene product records (to create annotations) and the use of GO annotation data in analysis tools together enable groups of similarly annotated gene products, within an "omics" dataset, to be identified as significantly enriched (18,24,25). Thus, dysregulated pathways, functions, and macromolecular complexes can be identified within high-throughput datasets.…”

Section: Gene Ontologymentioning

confidence: 99%

Gene Ontology: A Resource for Analysis and Interpretation of Alzheimer’s Disease Data

Kramarz

Lovering

2019

Alzheimer’s Disease

Self Cite

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Gene Ontology (GO) is a universal resource for analyses and interpretation of high-throughput biological datasets. GO is developed and curated by several different groups, based at scientific institutions around the world, working together under the auspices of the GO Consortium. GO annotations capture biological functional knowledge by associating gene products with GO terms. GO term and gene product records all have computer-readable accession numbers; therefore, these annotations can be easily used for analyses of large datasets while retaining human-readable labels. The UCL Functional Gene Annotation group focuses on GO annotation of human gene products. Our group has led initiatives to systematically annotate proteins and microRNAs across specific biomedical fields, and our current biocuration effort, funded by the Alzheimer' s Research UK foundation, is focused on dementia and Alzheimer' s disease. Our group has also contributed to the development and revision of the ontology describing neurological domains of biology. Here we present an overview of GO and explain how our work, as well as the work of other members of the GO Consortium, is improving the neurological domains of the GO resource. These biocuration efforts will benefit the dementia and Alzheimer' s research community by rendering GO more suitable for analyses of neurological datasets.

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“…2D-G, IM + Tan significantly reduced the number of invading cells and the wound closure rate compared with the IM (5 µM) and TIB-152 groups. Extracellular matrix degradation induced by MMPs is required for cell invasion and VEGF plays a key role in mediating cell migration (26,27). Therefore, western blotting was used to analyze the effects of Tan IIA and IM on the expression of VEGF and MMP-9.…”

Section: Tan Iia Enhances the Inhibitory Effect Of Im On Invasion Andmentioning

confidence: 99%

Tanshinone IIA enhances the inhibitory effect of imatinib on proliferation and motility of acute leukemia cell line TIB‑152 in�vivo and in�vitro by inhibiting the PI3K/AKT/mTOR signaling pathway

Teng¹,

Xu²,

Qin³

2019

Oncol Rep

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Acute lymphoblastic leukemia (ALL) is a malignant hematological disease. Tanshinone IIA (Tan IIA) has antitumor activity in vitro and in vivo. The aim of the present study was to investigate the effects of Tan IIA in combination with imatinib (IM) on the proliferation, apoptosis, migration and invasion of acute T lymphocytic leukemia TIB-152 cells in vivo and in vitro, and analyze the potential underlying mechanism. Tan IIA and IM, alone and in combination, significantly inhibited proliferation, migration and invasion of TIB-152 cells, and promoted apoptosis; the effect of co-treatment with Tan IIA plus IM was enhanced. IGF-1 promoted the proliferation, migration and invasion of TIB-152 cells and inhibited apoptosis, while Tan IIA treatment significantly reversed these effects. In vivo experiments demonstrated that treatment with Tan IIA and IM, alone or in combination, significantly inhibited tumor growth in TIB-152 xenograft mice; the growth inhibition of Tan IIA plus IM was the strongest observed. Western blot analysis revealed that the combination of Tan IIA and IM resulted in significantly lower levels of p-PI3K, p-AKT and p-mTOR in cells and tissues compared with the IM and Tan alone treatment groups. In addition, the combination of Tan IIA and IM significantly decreased the levels of Ki67, cleaved caspase-3, VEGF and MMP-9 in cells and tissues, and the level of caspase-3 was significantly increased. Taken together, the results revealed that Tan IIA enhanced the inhibitory effect of imatinib on TIB-152 cell proliferation, migration and invasion, and induced apoptosis, which may be associated with inhibition of the PI3K/AKT/mTOR signaling pathway. Tanshinone IIA enhances the inhibitory effect of imatinib on proliferation and motility of acute leukemia cell line TIB-152 in vivo and in vitro by inhibiting the PI3K/AKT/mTOR signaling pathway

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Vascular Endothelial Growth Factor (VEGF) Promotes Assembly of the p130Cas Interactome to Drive Endothelial Chemotactic Signaling and Angiogenesis

Cited by 28 publications

References 52 publications

Downregulation of IQGAP1 inhibits epithelial‐mesenchymal transition via the HIF1α/VEGF‐A signaling pathway in gastric cancer

Downregulation of IQGAP1 inhibits epithelial‐mesenchymal transition via the HIF1α/VEGF‐A signaling pathway in gastric cancer

Gene Ontology: A Resource for Analysis and Interpretation of Alzheimer’s Disease Data

Tanshinone IIA enhances the inhibitory effect of imatinib on proliferation and motility of acute leukemia cell line TIB‑152 in�vivo and in�vitro by inhibiting the PI3K/AKT/mTOR signaling pathway

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