Akt Phosphorylation Orchestrates T11TS Mediated Cell Cycle Arrest in Glioma Cells.
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.
Mesh Terms:
Animals, Brain Neoplasms, CD58 Antigens, Cell Cycle Checkpoints, Cyclin-Dependent Kinase Inhibitor p21, Female, Glioma, Male, PTEN Phosphohydrolase, Phosphorylation, Proto-Oncogene Proteins c-akt, Proto-Oncogene Proteins c-mdm2, Rats, Rats, Wistar, Tumor Microenvironment, Tumor Suppressor Protein p53, bcl-Associated Death Protein
Animals, Brain Neoplasms, CD58 Antigens, Cell Cycle Checkpoints, Cyclin-Dependent Kinase Inhibitor p21, Female, Glioma, Male, PTEN Phosphohydrolase, Phosphorylation, Proto-Oncogene Proteins c-akt, Proto-Oncogene Proteins c-mdm2, Rats, Rats, Wistar, Tumor Microenvironment, Tumor Suppressor Protein p53, bcl-Associated Death Protein
Cancer Invest
Date: Nov. 01, 2021
PubMed ID: 34569407
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