Fen Yang
Sun Yat-sen University
9 Papers
89 Citations
Fen Yang is an academic researcher from Sun Yat-sen University. The author has contributed to research in topics: Protein kinase B & PI3K/AKT/mTOR pathway. The author has an hindex of 6, co-authored 9 publications. Previous affiliations of Fen Yang include Zhejiang University & Nanjing Medical University.
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Papers
Hirsutanol A, a novel sesquiterpene compound from fungus Chondrostereum sp., induces apoptosis and inhibits tumor growth through mitochondrial-independent ROS production: Hirsutanol A inhibits tumor growth through ROS production
Fen Yang,Wen Dan Chen,Rong Deng,Hui Zhang,Jun Tang,Ke Wei Wu,Dan Dan Li,Gong Kan Feng,Wen-Jian Lan,Hou-Jin Li,Xiao Feng Zhu +10 more
TL;DR: In this paper, the antitumor activity of hirsutanol A and its molecular mechanisms were investigated, and it was shown that hirsutsanol A exhibited potent cytotoxic effect on many kinds of cancer cell lines.
Hirsutanol A induces apoptosis and autophagy via reactive oxygen species accumulation in breast cancer MCF-7 cells.
Fen Yang,Fen Yang,Wen Dan Chen,Rong Deng,Dan Dan Li,Ke Wei Wu,Gong Kan Feng,Hou-Jin Li,Xiao Feng Zhu +8 more
TL;DR: The results showed that hirsutanol A could inhibit cell proliferation, elevate reactive oxygen species (ROS) level, and induce apoptosis and autophagy and co-treatment with an autophagic inhibitor could sensitize MCF-7 cells to hirsUTanol A.
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Inhibition of DNA methyltransferase as a novel therapeutic strategy to overcome acquired resistance to dual PI3K/mTOR inhibitors.
Xiao Jun Qian,Yun Tian Li,Yan Yu,Fen Yang,Fen Yang,Rong Deng,Jiao Ji,Lin Jiao,Xuan Li,Rui Yan Wu,Wen Dan Chen,Gong Kan Feng,Xiao Feng Zhu +12 more
TL;DR: It is demonstrated that DNA methyltransferase is a key modulator and a common node upstream of the AKT/mTOR and PDK1/MYC pathways, which are activated in cancer cells with acquired BEZ235 resistance, suggesting the potential clinical application of this strategy to overcome BEz235 resistance.
DC120, a Novel and Potent Inhibitor of AKT Kinase, Induces Tumor Cell Apoptosis and Suppresses Tumor Growth
TL;DR: The results showed that DC120 could obviously inhibit the proliferation of CNE2 and MDA-MB-453 cells via induction of apoptosis and partially attenuated the phosphorylation levels of forkhead transcription factor, FKHRL1, glycogen synthase kinase 3β, and mammalian target of rapamycin in a dose-dependent and time-dependent fashion and led to an increase in the nuclear accumulation of exogenous FKHR in cancer cells.
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Abstract C86: DC120, a novel and potent inhibitor of AKT kinase, induces tumor cells apoptosis and suppresses tumor growth.
TL;DR: In vivo experiments showed DC120 at 20 mg/kg/qd remarkably inhibited the CNE2 xenograft tumor growth with the T/C value of 36.1%, accompanied by increasing TUNEL-positve cells in tumor sample, and data provide validation for the development of DC120 to treat cancers displaying elevated levels of AKT.