VEGF targets the tumour cell

Goel, Hira Lal; Mercurio, Arthur M.

doi:10.1038/nrc3627

Cited by 1,055 publications

(874 citation statements)

References 188 publications

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“…103 In addition, VEGFA was also shown to directly act on tumor cells by promoting survival, proliferation, migration and invasion. 104 In a potential scenario radiotherapy induces hypoxia which in turn triggers tenascin-C and VEGFA expression. Each molecule/pathway alone as well as in conjunction may promote new blood vessel formation and tumor cell survival, thus promoting tumor regrowth, progression and metastasis post irradiation (Fig.…”

Section: Induction Of Tenascin-c Upon Radiotherapymentioning

confidence: 99%

Tenascin-C: Exploitation and collateral damage in cancer management

Spenlé

Saupe

Midwood³

et al. 2015

Cell Adhesion & Migration

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Section: Induction Of Tenascin-c Upon Radiotherapymentioning

confidence: 99%

Tenascin-C: Exploitation and collateral damage in cancer management

Spenlé

Saupe

Midwood³

et al. 2015

Cell Adhesion & Migration

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“…Bevacizumab is a monoclonal antibody against VEGF that inhibits tumor angiogenesis and growth by blocking VEGF–VEGFR binding on endothelial cells, which is commonly used for the treatment of metastatic BC. To date, accumulating evidence has shown that VEGF is a multifunction molecule that affects a variety of cells in the tumor microenvironment, not only in endothelial cells 5. Thus, in the current study, we hypothesized that VEGF has a direct effect on BC cells that contributes to their malignant behavior.…”

Section: Discussionmentioning

confidence: 93%

“…In addition, hypoxia induced by anti‐angiogenic therapy promotes selection of aggressive cancer cells17 and expansion of cancer stem cell pool 18. According to recent studies, VEGF is a multifunction molecule targeting not only endothelial cells but also other cell members in the tumor microenvironment, including cancer cells, fibroblasts, immune cells and more 5. However, VEGF's direct effect on cancer cells is not yet fully understood.…”

Section: Introductionmentioning

confidence: 99%

Long isoform of VEGF stimulates cell migration of breast cancer by filopodia formation via NRP1/ARHGAP17/Cdc42 regulatory network

Kiso

Tanaka

Toi

et al. 2018

Intl Journal of Cancer

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VEGF stimulates endothelial cells as a key molecule in angiogenesis. VEGF also works as a multifunction molecule, which targets a variety of cell members in the tumor microenvironment. We aimed to reveal VEGF‐related molecular mechanisms on breast cancer cells. VEGF‐knocked‐out MDA‐MB‐231 cells (231VEGFKOex3) showed rounded morphology and shorter perimeter (1.6‐fold, p < 0.0001). The 231VEGFKOex3 cells also showed impaired cell migration (2.6‐fold, p = 0.002). Bevacizumab treatment did not induce any change in morphology and mobility. Soluble neuropilin‐1 overexpressing MDA‐MB‐231 cells (231sNRP1) exhibited rounded morphology and shorter perimeter (1.3‐fold, p < 0.0001). The 231sNRP1 cells also showed impaired cell migration (1.7‐fold, p = 0.003). These changes were similar to that of 231VEGFKOex3 cells. As MDA‐MB‐231 cells express almost no VEGFR, these results indicate that the interaction between NRP1 and long isoform of VEGF containing a NRP‐binding domain regulates the morphology and migration ability of MDA‐MB‐231 cells. Genome‐wide gene expression profiling identified ARHGAP17 as one of the target genes in the downstream of the VEGF/NRP1 signal. We also show that VEGF/NRP1 signal controls filopodia formation of the cells by modulating Cdc42 activity via ARHGAP17. Among 1,980 breast cancer cases from a public database, the ratio of VEGF and SEMA3A in primary tumors (n = 450) of hormone‐receptor‐negative breast cancer is associated with ARHGAP17 expression inversely, and with disease free survival. Altogether, the bevacizumab‐independent VEGF/NRP1/ARHGAP17/Cdc42 regulatory network plays important roles in malignant behavior of breast cancer.

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“…Several studies revealed that VEGF165 was highly expressed in breast cancer tissues compared with adjacent tissues (23,24). RT-qPCR experiments demonstrated that four isoforms of VEGF were expressed in human breast cancer tissues, including VEGF121, VEGF145, VEGF165 and VEGF189, being VEGF165 the most abundant one (25). In addition, previous studies demonstrated that VEGF165 fused to GFP at its C-terminus was secreted and biologically active (26).…”

Section: Discussionmentioning

confidence: 99%

Construction and expression of a lentivirus expression vector carrying the VEGF165-EGFP fusion gene in breast cancer MCF-7 cells

Luo¹,

Huang²,

Hou³

et al. 2017

Oncology Letters

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Abstract. Vascular endothelial growth factor (VEGF)165 is one of the most abundant and potent angiogenic factors in both physiological and pathological conditions. However, the function and mechanism of VEGF165 in tumors and their environment remain to be elucidated. In the present study, a lentivirus vector (LV) that contained the VEGF165-enhanced green fluorescent protein (EGFP) fusion gene was constructed and transfected into the human breast cancer cell line MCF-7. Following transfection, the expression of VEGF165 in MCF-7 cells was detected by reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and western blotting. Further cellular localization of VEGF165 was observed through fluorescence microscopy. The titer of the recombinant lentivirus was 5.44x10 7 TU/ml in the LV-VEGF165-EGFP group and 5.00x10 8 TU/ml in the LV-EGFP negative control group. RT-qPCR and western blotting demonstrated that the expression of VEGF165 was significantly increased in the LV-VEGF165-EGFP group compared with the control group. The present study lays the foundation for in vitro and in vivo studies on tumor cell derived-VEGF165. Furthermore, the present fusion gene expression vector may provide a potential approach for gene therapy treatment of cancer and other diseases that require regulation of angiogenesis.

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VEGF targets the tumour cell

Cited by 1,055 publications

References 188 publications

Tenascin-C: Exploitation and collateral damage in cancer management

Tenascin-C: Exploitation and collateral damage in cancer management

Long isoform of VEGF stimulates cell migration of breast cancer by filopodia formation via NRP1/ARHGAP17/Cdc42 regulatory network

Construction and expression of a lentivirus expression vector carrying the VEGF165-EGFP fusion gene in breast cancer MCF-7 cells

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