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YC-1 inhibits HIF-1 expression in prostate cancer cells: contribution of Akt/NF-kappaB signaling to HIF-1alpha accumulation during hypoxia.
YC-1 is a novel antitumor agent that inhibits HIF-1 through previously unexplained mechanisms and is found to suppress the PI3K/Akt/mTOR/4E-BP pathway, which serves to regulate Hif-1alpha expression at the translational step.
Antroquinonol displays anticancer potential against human hepatocellular carcinoma cells: a crucial role of AMPK and mTOR pathways.
Investigation of ouabain-induced anticancer effect in human androgen-independent prostate cancer PC-3 cells.
Targeting Energy Metabolic and Oncogenic Signaling Pathways in Triple-negative Breast Cancer by a Novel Adenosine Monophosphate-activated Protein Kinase (AMPK) Activator*
- Kuen-Haur Lee, E. Hsu, C. Chen
- Biology, MedicineThe Journal of Biological Chemistry
- 14 September 2011
OSU-53 is a potent, orally bioavailable AMPK activator that acts through a broad spectrum of antitumor activities downstream of AMPK activation and modulated relevant intratumoral biomarkers of drug activity.
YC-1 inhibits HIF-1 expression in prostate cancer cells: contribution of Akt/NF-κB signaling to HIF-1α accumulation during hypoxia
YC-1 is a novel antitumor agent that inhibits HIF-1 through previously unexplained mechanisms, and is found to suppress the PI3K/Akt/mTOR/4E-BP pathway, which serves to regulate Hif-1α expression at the translational step.
Genistein induces apoptosis in human hepatocellular carcinomas via interaction of endoplasmic reticulum stress and mitochondrial insult.
Antiplatelet Effect of Gingerol Isolated from Zingiber officinale
The purpose of this investigation was to determine the antiplatelet mechanism of gingerol.
Esculetin inhibits Ras-mediated cell proliferation and attenuates vascular restenosis following angioplasty in rats.
Pharmacological evaluation of several major ingredients of Chinese herbal medicines in human hepatoma Hep3B cells.
Development of novel adenosine monophosphate-activated protein kinase activators.
Evidence indicates that this drug-induced suppression of LPS-stimulated IL-6 production was attributable to AMPK activation, and compound 53-mediated AM PK activation was demonstrated in C-26 colon adenocarcinoma cells, indicating that it is not a cell line-specific event.