scholarly journals Transcriptomic Profiling Revealed Plexin A2 Downregulation With Migration and Invasion Alteration in Dacarbazine-Treated Primary Melanoma Cells

2021 ◽  
Vol 11 ◽  
Author(s):  
Anna Tyumentseva ◽  
Anton Averchuk ◽  
Nadezhda Palkina ◽  
Ivan Zinchenko ◽  
Anton Moshev ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Cell Lines ◽  
Focal Adhesion ◽  
Melanoma Cells ◽  
Migration And Invasion ◽  
Cell Phenotype ◽  
Vascular Endothelial ◽  
Tumor Dissemination ◽  
Endothelial Growth Factor

Melanoma is highly heterogeneous type of malignant neoplasm that is responsible for the majority of deaths among other types of skin cancer. In the present study, we screened a list of differentially expressed genes in two primary, drug-naïve melanoma cell lines derived from patients with melanoma following treatment of the cells with the chemotherapeutic agent dacarbazine. The aim was to determine the transcriptomic profiles and associated alterations in the cell phenotype. We found the vascular endothelial growth factor A/vascular endothelial growth factor receptor 2, phosphoinositide 3-kinase/protein kinase B and focal adhesion signaling pathways to be top altered after dacarbazine treatment. In addition, we observed the expression levels of genes associated with tumor dissemination, integrin β8 and matrix metalloproteinase-1, to be diminished in both cell lines studied, the results of which were confirmed by reverse transcription-quantitative polymerase chain reaction. By contrast, plexin A2 expression was found to be upregulated in K2303 cells, where reduced migration and invasion were also observed, following dacarbazine treatment. Plexin A2 downregulation was associated with the promotion of migrative and invasive capacities in B0404 melanoma cells. Since plexin A2 is semaphorin co-receptor that is involved in focal adhesion and cell migration regulation, the present study suggested that plexin A2 may be implicated in the dacarbazine-mediated phenotypic shift of melanoma cells. We propose that the signature of cancer cell invasiveness can be revealed by using a combination of transcriptomic and functional approaches, which should be applied in the development of personalized therapeutic strategies for each patient with melanoma.

scholarly journals Synthetic Triterpenoid CDDO-Me Inhibits Proliferation, Migration, and Invasion in GBM8401 and GBM8901

2020 ◽  
Vol 104 (3-4) ◽  
pp. 90-98 ◽  
Author(s):  
Chih-Hui Chang ◽  
Hung-Pei Tsai ◽  
Shih-Hsun Kuo ◽  
Joon-Khim Loh ◽  
Chien-Ju Lin ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Cyclin D1 ◽  
Cell Lines ◽  
Migration And Invasion ◽  
Vascular Endothelial ◽  
Glioblastoma Cell ◽  
Endothelial Growth Factor ◽  
Glioblastoma Cell Lines

Objectives: We determined the anticancer potency of CDDO-Me in glioblastoma cell lines and the underlying mechanisms in vitro. Summary: CDDO-Me is a synthetic triterpenoid with more potent anticancer and cancer preventive actions compared with the original triterpenoid CDDO. Methods: Two glioblastoma cell lines, GBM8401 and GBM8901, were utilized to test the effect of CDDO-Me on cell viability, cell migration, and cell invasion using the MTT, wound healing, and transwell migration assays, respectively. Additionally, Western blotting was used to determine the protein expression levels of N-cadherin, cyclin D1, and vascular endothelial growth factor. Results: At nanomolar concentrations, CDDO-Me inhibited proliferation, migration, and invasion in both cell lines. In addition, CDDO-Me exhibited a dose-dependent downregulation in the protein levels of N-cadherin, cyclin D1, and vascular endothelial growth factor in GBM8401 and GBM8901 cells. Conclusions: CDDO-Me exhibited anticancer effects at low nanomolar concentrations and should be considered as a potential chemotherapeutic agent for glioblastoma.

scholarly journals Human Melanoma Cells Secrete and Respond to Placenta Growth Factor and Vascular Endothelial Growth Factor

2000 ◽  
Vol 115 (6) ◽  
pp. 1000-1007 ◽  
Author(s):  
Pedro M. Lacal ◽  
Cristina M. Failla ◽  
Elena Pagani ◽  
Teresa Odorisio ◽  
Cataldo Schietroma ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Melanoma Cells ◽  
Human Melanoma ◽  
Vascular Endothelial ◽  
Placenta Growth Factor ◽  
Human Melanoma Cells ◽  
Endothelial Growth Factor

scholarly journals Honokiol: A Review of Its Anticancer Potential and Mechanisms

Cancers ◽  
2019 ◽  
Vol 12 (1) ◽  
pp. 48 ◽  
Author(s):  
Chon Phin Ong ◽  
Wai Leong Lee ◽  
Yin Quan Tang ◽  
Wei Hsum Yap
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Natural Products ◽  
Cell Migration ◽  
Growth Factor ◽  
Migration And Invasion ◽  
Vascular Endothelial ◽  
Mesenchymal Transition ◽  
Chemical Structures ◽  
Endothelial Growth Factor ◽  
Promising Source

Cancer is characterised by uncontrolled cell division and abnormal cell growth, which is largely caused by a variety of gene mutations. There are continuous efforts being made to develop effective cancer treatments as resistance to current anticancer drugs has been on the rise. Natural products represent a promising source in the search for anticancer treatments as they possess unique chemical structures and combinations of compounds that may be effective against cancer with a minimal toxicity profile or few side effects compared to standard anticancer therapy. Extensive research on natural products has shown that bioactive natural compounds target multiple cellular processes and pathways involved in cancer progression. In this review, we discuss honokiol, a plant bioactive compound that originates mainly from the Magnolia species. Various studies have proven that honokiol exerts broad-range anticancer activity in vitro and in vivo by regulating numerous signalling pathways. These include induction of G0/G1 and G2/M cell cycle arrest (via the regulation of cyclin-dependent kinase (CDK) and cyclin proteins), epithelial–mesenchymal transition inhibition via the downregulation of mesenchymal markers and upregulation of epithelial markers. Additionally, honokiol possesses the capability to supress cell migration and invasion via the downregulation of several matrix-metalloproteinases (activation of 5′ AMP-activated protein kinase (AMPK) and KISS1/KISS1R signalling), inhibiting cell migration, invasion, and metastasis, as well as inducing anti-angiogenesis activity (via the down-regulation of vascular endothelial growth factor (VEGFR) and vascular endothelial growth factor (VEGF)). Combining these studies provides significant insights for the potential of honokiol to be a promising candidate natural compound for chemoprevention and treatment.

scholarly journals Src-mediated coupling of focal adhesion kinase to integrin αvβ5 in vascular endothelial growth factor signaling

2002 ◽  
Vol 157 (1) ◽  
pp. 149-160 ◽  
Author(s):  
Brian P. Eliceiri ◽  
Xose S. Puente ◽  
John D. Hood ◽  
Dwayne G. Stupack ◽  
David D. Schlaepfer ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Focal Adhesion Kinase ◽  
Focal Adhesion ◽  
Critical Event ◽  
Growth Factor Signaling ◽  
Vascular Endothelial ◽  
Signaling Complex ◽  
Specific Growth Factor ◽  
Endothelial Growth Factor

Vascular endothelial growth factor (VEGF) promotes vascular permeability (VP) and neovascularization, and is required for development. We find that VEGF-stimulated Src activity in chick embryo blood vessels induces the coupling of focal adhesion kinase (FAK) to integrin αvβ5, a critical event in VEGF-mediated signaling and biological responsiveness. In contrast, FAK is constitutively associated with β1 and β3 integrins in the presence or absence of growth factors. In cultured endothelial cells, VEGF, but not basic fibroblast growth factor, promotes the Src-mediated phosphorylation of FAK on tyrosine 861, which contributes to the formation of a FAK/αvβ5 signaling complex. Moreover, formation of this FAK/αvβ5 complex is significantly reduced in pp60c-src-deficient mice. Supporting these results, mice deficient in either pp60c-src or integrin β5, but not integrin β3, have a reduced VP response to VEGF. This FAK/αvβ5 complex was also detected in epidermal growth factor-stimulated epithelial cells, suggesting a function for this complex outside the endothelium. Our findings indicate that Src can coordinate specific growth factor and extracellular matrix inputs by recruiting integrin αvβ5 into a FAK-containing signaling complex during growth factor–mediated biological responses.

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