Role of Sulindac and Celecoxib in the regulation of angiogenesis during the early neoplasm of colon: Exploring PI3-K/PTEN/Akt pathway to the canonical Wnt/β-catenin signaling
作者： Vivek Vaish , Sankar Nath Sanyal , None
DOI: 10.1016/J.BIOPHA.2012.01.004
关键词:
摘要: Angiogenesis refers to the generation of new blood vasculature from nearby pre-existing one and is regulated by a balance between pro- anti-angiogenic factors. During carcinogenesis, pro-angiogenic factors dominate initialize growth capillaries provide nutrition, overcome hypoxia inside tumor microenvironment. In present study, we have observed role Phosphatidylinositol-3-kinase (PI3-K)/Phophatase tensin homolog deleted on chromosome ten (PTEN)/Akt (Protein kinase B) pathway canonical Wnt/β-catenin downstream signaling in regulation various molecules including vascular endocrine factor-A (VEGF-A), matix metalloproteinases (MMPs), inducible nitric oxide synthase (iNOS) chemokines for progression experimental colorectal cancer with 1,2-dimethylhydrazine dihydrochloride (DMH) effects two non-steroidal anti-inflammatory drugs (NSAIDs) viz. Sulindac Celecoxib. Morphological histopathological studies were performed analyze tumorigenic modifications while flow cytometry relative quantification apoptotic events. Transcriptional translational biomolecules analyzed via Reverse Transcriptase-and quantitative Real Time PCR, Western immoblotting immunoflurescence, respectively. vitro phosphorylation, gelatin zymography (NO) assay observe activation states Akt, MMPs iNOS enzyme, Dysregultion Akt activation, thereby, aberrant β-catenin along production NO could positively regulate angiogenesis. NSAIDs can these carcinogenic controlling key check points higher PTEN glycogen kinase-3β (GSK-3β) expression repressing inducing apoptosis among cells.
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