IndraLab

Statements


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"Given our hypothesis that IKKbeta promotes KRAS induced angiogenesis, which relies on KRAS induced VEGF and IL-8 secretion [XREF_BIBR, XREF_BIBR], and given that VEGF and IL-8 are transcriptional targets of NF-kappaB [XREF_BIBR], a transcription factor activated by oncogenic KRAS in the lung in an IKKbeta dependent manner [XREF_BIBR], we decided to investigate whether IKKbeta targeting would affect VEGF and IL-8 expression."

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"Taken together, these results provide a novel mechanistic understanding of how the IKKbeta pathway affects human lung tumorigenesis, indicating that IKKbeta promotes KRAS induced angiogenesis both by cancer cell-intrinsic and cancer cell independent mechanisms, which strongly suggests IKKbeta inhibition as a promising antiangiogenic approach to be explored for KRAS induced lung cancer therapy."

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"K-Ras Promotes Angiogenesis Mediated by Immortalized Human Pancreatic Epithelial Cells through Mitogen Activated Protein Kinase Signaling Pathways."

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"Similar results were obtained using another pair of immortalized human pancreatic duct derived cells, E6/E7/st and its oncogenic K-Ras variant, E6/E7/Ras/st. Taken together, our results suggest that angiogenesis is initiated by paracrine epithelial secretion of CXC chemokines and VEGF downstream of activated oncogenic K-Ras, and that this vascular maturation is in part dependent on MEK1/2 and c-Jun signaling."

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"Taken together, these results suggest that IKKbeta is an important mediator of KRAS induced angiogenesis, and that IKKbeta promotes angiogenesis both by cancer cell dependent and -independent mechanisms."

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"Even though pathological angiogenesis in this model is not induced by KRAS, it can result in activation of the IKK and NF-kappaB pathway due to the relative hypoxia induced by the change in oxygen levels."

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"PDAC often harbors the universal mutations in the proto-oncogene K-RAS (>90% prevalence in pancreatic cancer), which persistently accelerates and activates various oncogenic events (e.g., uncontrolled proliferation, sustained angiogenesis, metastasis, or invasion), thus leading to metabolic reprogramming and resistance to cell death [1, 2]."

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"In conclusion, we have identified IKKbeta as a mediator of KRAS induced angiogenesis in lung cancer in part by promoting secretion of proangiogenic factors VEGF and IL-8."

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"GSEA identified a number of biological states and processes overrepresented in the glioblastoma infiltrating CD14 + cells relative to those in CD14 + blood cells, including signaling by KRAS, TGF-beta, and TNF-alpha; epithelial-mesenchymal transition; angiogenesis; coagulation; the G 2 / M cell cycle checkpoint; and hypoxia (XREF_FIG)."

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"Targeting oncogenic KRAS in non small cell lung cancer cells by phenformin inhibits growth and angiogenesis."
Mutated KRAS activates angiogenesis. 5 / 5
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"It is supposed that the KRAS mutation might activate angiogenesis in several ways : by increasing production of VEGF and CXCL-8 (proangiogenetic interleukin 8) and by activating growth of the tumour cells (30, 31)."

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"Activating KRAS mutation in carcinoma cells may induce angiogenesis via several mechanisms."

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"Kras mutation can induce proliferation of tumor cell, angiogenesis and some adverse events such as invasion or metastasis."

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"Previous research has shown that KRAS mutations support the production of VEGF and the decline of angiogenesis inhibitor thrombospondin."

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"ADS and EC share several altered molecular pathways, such as high level of vascular endothelial growth factor, platelet-derived growth factor, increased production of reactive species of oxygen and pro-inflammatory cytokines, KRAS mutations [31], which lead to increased angiogenesis, abnormal tissue growth, and invasion [32]."
KRAS-G12V activates angiogenesis. 1 / 1
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"KRAS G12V expression in the TbetaR cell line induced processes involved with Wnt and JAK and STAT signaling, angiogenesis, and motility, and downregulated genes involved in apoptosis, adhesion, and ECM."
GTP-bound active KRAS activates angiogenesis. 1 / 1
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"The angiogenic switch can be induced at a predictable time and usually more rapidly, by introduction of oncogenes into the tumors. When the human non-angiogenic osteosarcoma was transfected with the ras oncogene, neovascularized tumors appeared within 2 weeks [7]."