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- W975366408 abstract "Angiogenesis is crucial for breast tumor growth and metastasis. Regulated pattern of endothelial cell survival and death play a central role in the timely evolution and regression of angiogenic responses. We have shown that dolichol-linked oligosaccharide (i.e., LLO) biosynthesis and turnover are required for angiogenesis. Investigating the efficacy of a LLO biosynthetic inhibitor tunicamycin for anti-angiogenetic breast cancer therapy indicates cell cycle arrest in G1 and induction of apoptosis by unfolded protein response (upr) signaling. This paralleled upregulation of c-Jun, c-Myc and down regulation of c-fos. Upregulated p53 expression indicated failure of cell survival. IGF-1 (20ng/ml) addition exhibited no change in the cell status as confirmed by down regulation of PI3KR, pAkt and p53(S14). This is supported by down regulation of phospho Akt (473)/Akt (308), GSK3 beta, phosphocaspase-9, phospho-Bad and phospho mTOR expression. Changes in NFkB phosphorylation (S14) however remained silent. QRT-PCR confirmed upregulation of GRP-78, Bcl-2, caspase-3, p53 expression and down regulation of PI3KR following IGF-1 challenges in tunicamycin treated cells. IGF-1 signaling triggers glucose uptake for energy metabolism but ATP level could not be raised when tunicamycin was present. This strongly suggested that tunicamycin down regulates the PI3-K/AKt signaling of cell survival and could help developing glycotherapeutic for treating breast cancer. Supported by NIH/NCRR/RCMI G12-RR03035 (KB); NIH U54-CA096297 and Komen for the Cure BCTR06582 (DKB)." @default.
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- W975366408 date "2010-04-01" @default.
- W975366408 modified "2023-10-02" @default.
- W975366408 title "Unfolded protein response interferes IGF‐1 signaling of capillary endothelial cell survival" @default.
- W975366408 doi "https://doi.org/10.1096/fasebj.24.1_supplement.695.2" @default.
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