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Santi, SA and Lee, H (2011) Ablation of Akt2 induces autophagy through cell cycle arrest, the downregulation of p70S6K, and the deregulation of mitochondria in MDA-MB231 cells. PLoS ONE 6:e14614
Akt/PKB is a promising anticancer therapeutic target, since abnormally elevated Akt activity is directly correlated to tumor development, progression, poor prognosis and resistance to cancer therapies. Currently, the unique role of each Akt isoform and their relevance to human breast cancer are poorly understood.
Autophagy/drug effects; Autophagy/genetics; Breast Neoplasms/pathology; Cell Cycle; Cell Cycle Proteins; Cell Line, Tumor; Cell Proliferation; Cell Survival; Down-Regulation; Drug Delivery Systems/methods; Female; Humans; Mitochondria/pathology; Protein Isoforms; Proto-Oncogene Proteins c-akt/deficiency; Proto-Oncogene Proteins c-akt/genetics; RNA, Small Interfering/pharmacology; Ribosomal Protein S6 Kinases, 70-kDa/genetics
|Gene product||Qualifier||GO Term||Evidence Code||with/from||Aspect||Extension||Notes||Status|
|GO:2000144: positive regulation of DNA-dependent transcription, initiation||
Figure 2A shows that the use of AKT2 siRNA, causes a decrease in the transcriptional levels of Cdk2, while scrambled or uninhibited AKT2 allows for transcriptional up-regulation of Ckd2.
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