ArticleCancer cell international2014
Anti-tumor effect of a novel PI3-kinase inhibitor, SF1126, in (12) V-Ha-Ras transgenic mouse glioma model.
Article in Cancer cell international, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 21 citations in OpenAlex.
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- MYCN Impact on High-Risk Neuroblastoma: From Diagnosis and Prognosis to Targeted Treatment.Cancers · 2022Review
- Targeting the Tumor Microenvironment in Neuroblastoma: Recent Advances and Future Directions.Cancers · 2020Review
- AnnexinA5 promote glioma cell invasion and migration via the PI3K/Akt/NF-κB signaling pathway.Journal of neuro-oncology · 2018Article
- Retinoblastoma protein (Rb) links hypoxia to altered mechanical properties in cancer cells as measured by an optical tweezer.Scientific reports · 2017Article
- Association of high microvessel αOncotarget · 2017Article
- Single Agent and Synergistic Activity of the "First-in-Class" Dual PI3K/BRD4 Inhibitor SF1126 with Sorafenib in Hepatocellular Carcinoma.Molecular cancer therapeutics · 2016Article
- miR-222 attenuates cisplatin-induced cell death by targeting the PPP2R2A/Akt/mTOR Axis in bladder cancer cells.Journal of cellular and molecular medicine · 2016Article
- New perspectives in glioblastoma antiangiogenic therapy.Contemporary oncology (Poznan, Poland) · 2016Review
- PI-3K Inhibitors Preferentially Target CD15+ Cancer Stem Cell Population in SHH Driven Medulloblastoma.PloS one · 2016Article
- Systemic modeling myeloma-osteoclast interactions under normoxic/hypoxic condition using a novel computational approach.Scientific reports · 2015Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundGrowth factor mediated activation of RAS-MAP-kinase and PI3-kinase-AKT pathways are critical for the pathogenesis of glioblastoma. The attenuation of PI3-kinase/AKT signaling will be effective in regulating the tumorigenic phenotypes of the glioma cells.
methodsGlioma cells derived from the brain of the (12) V-Ha-Ras transgenic mice were used to study the effect of PI-3 kinase inhibitor SF1126 on activation of AKT and ERK signaling, proliferation, vitronectin mediated migration and changes in the distribution of cortical actin on vitronectin in the glioma cells in vitro. The anti-tumor effects of SF1126 were also tested in vivo using pre-established tumors (subcutaneous injection of the glioma cells from (12) V-Ha-Ras transgenic mice) in a mouse xenograft model.
resultsOur results demonstrate that treatment of LacZ+, GFAP + and PCNA + (12) V-Ras Tg transformed astrocytes with SF1126 and LY294002 blocked the activation of AKT as well as EGF-induced phospho-ERK. Most notably, treatment of SF1126 blocked integrin-dependent migration in transwell and scratch assays and caused a significant change in the organization and distribution of cortical actin on vitronectin in the glioma cells. Moreover, SF1126 treatment inhibited in vitro proliferation of these cells and in vivo growth of pre-established subcutaneous tumors in a xenograft model.
conclusionThe present study validate the potent anti-proliferative and anti-migratory activity of SF1126, in a V(12) Ras oncogene driven glioma model and suggest that this effect is mediated potentially through a combined attenuation of PI3-kinase and MAP-kinase signaling pathways.
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