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AMP-activated Protein Kinase Activity Is Critical for Hypoxia-inducible Factor-1 Transcriptional Activity and Its Target Gene Expression under Hypoxic Conditions in DU145 Cells*
It is demonstrated that hypoxia or CoCl2 rapidly activated AMPK in DU145 human prostate cancer cells, and its activation preceded the induction of Hif-1α expression, indicating that AMPK is critical for the HIF-1 transcriptional activity and its target gene expression.
Reactive oxygen species stabilize hypoxia-inducible factor-1 alpha protein and stimulate transcriptional activity via AMP-activated protein kinase in DU145 human prostate cancer cells.
Findings identify AMPK as a key determinant of HIF-1 functions in response to ROS and its possible role in the sophisticated Hif-1 regulatory mechanisms.
Ginkgetin inhibits the growth of DU−145 prostate cancer cells through inhibition of signal transducer and activator of transcription 3 activity
This is the first report that ginkgetin exerts antitumor activity by inhibiting STAT3, and may be a useful lead molecule for development of a therapeutic STAT3 inhibitor.
Antidiabetes and Antiobesity Effect of Cryptotanshinone via Activation of AMP-Activated Protein Kinase
The findings suggest that the activation of the AMPK pathway might contribute to the development of novel therapeutic approaches for the treatment of metabolic disorders such as type 2 diabetes and obesity.
LAMB3 mediates metastatic tumor behavior in papillary thyroid cancer by regulating c-MET/Akt signals
The results suggest that LAMB3 leads to tumor invasion via Akt activation induced by the HGF/c-MET axis in papillary thyroid cancer cells.
AMP-activated protein kinase activity is required for vanadate-induced hypoxia-inducible factor 1alpha expression in DU145 cells.
It is demonstrated that AMPK was rapidly activated in response to vanadate in DU145 human prostate carcinoma, and that its activation preceded HIF-1alpha expression, suggesting that AM PK is a novel and critical component of Hif-1 regulation.
HOXB5 acts as an oncogenic driver in head and neck squamous cell carcinoma via EGFR/Akt/Wnt/β-catenin signaling axis.