Abstract
The novel anti-neoplastic glycopeptide T11TS retards glioma both in in-vitro clinical samples and in-vivo models. This study investigates the correlation between altering the glioma microenvironment with glioma arrest and death. Flow cytometry, immunoblotting, ELISA, and co-immunoprecipitation were employed to investigate glioma cell arrest and death. Results include a decline in phosphorylation of Akt and attenuation of p21 phosphorylation (Thr145,Ser146) and disassociation of p-Akt-Mdm2 and p-Akt-BAD facilitating death by Akt>BAD. T11TS influence phosphorylation patterns in two focal axes Akt>p21 and Akt>Mdm2>p53. The current article provides crucial insight in deciphering the mechanism of T11TS induced glioma cell arrest and death.
Keywords:
Akt; Glioma; T11TS; apoptosis; cell cycle arrest.
MeSH terms
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Animals
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Brain Neoplasms / drug therapy*
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Brain Neoplasms / metabolism
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Brain Neoplasms / pathology
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CD58 Antigens / pharmacology*
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CD58 Antigens / therapeutic use
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Cell Cycle Checkpoints / drug effects
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Cyclin-Dependent Kinase Inhibitor p21 / metabolism
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Female
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Glioma / drug therapy*
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Glioma / metabolism
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Glioma / pathology
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Male
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PTEN Phosphohydrolase / analysis
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Phosphorylation
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Proto-Oncogene Proteins c-akt / metabolism*
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Proto-Oncogene Proteins c-mdm2 / analysis
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Rats
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Rats, Wistar
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Tumor Microenvironment
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Tumor Suppressor Protein p53 / analysis
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bcl-Associated Death Protein / metabolism
Substances
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CD58 Antigens
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CDKN1A protein, human
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Cyclin-Dependent Kinase Inhibitor p21
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T11TS protein, sheep
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Tumor Suppressor Protein p53
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bcl-Associated Death Protein
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Proto-Oncogene Proteins c-mdm2
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Proto-Oncogene Proteins c-akt
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PTEN Phosphohydrolase