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Shi-Hao Tan

Researcher at National University of Singapore

Publications -  16
Citations -  1030

Shi-Hao Tan is an academic researcher from National University of Singapore. The author has contributed to research in topics: Autophagy & Programmed cell death. The author has an hindex of 9, co-authored 11 publications receiving 858 citations.

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Activation of lysosomal function in the course of autophagy via mTORC1 suppression and autophagosome-lysosome fusion

TL;DR: It is found that suppression of mammalian target of rapamycin activity by starvation or two mTOR catalytic inhibitors (PP242 and Torin1), but not by an allosteric inhibitor (rapamycin), leads to activation of lysosomal function.
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Induction of Autophagy by Palmitic Acid via Protein Kinase C-mediated Signaling Pathway Independent of mTOR (Mammalian Target of Rapamycin)

TL;DR: It is found that PA, but not oleic acid, was able to cause an increase in autophagic flux, evidenced by LC3-II accumulation and formation of GFP-LC3 puncta, and inhibition of autophagy sensitized the cells to PA-induced apoptosis, suggesting the pro-survival function ofautophagy induced by PA.
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Histone deacetylase inhibitors induce autophagy through FOXO1-dependent pathways

TL;DR: The studies reveal a novel function of FOXO1 in HDACIs-mediated autophagy in human cancer cells and thus support the development of a novel therapeutic strategy by combining HDACs and autophagic inhibitors in cancer therapy.
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Artesunate Induces Cell Death in Human Cancer Cells via Enhancing Lysosomal Function and Lysosomal Degradation of Ferritin

TL;DR: This study demonstrates that ART treatment activates lysosomal function and then promotes ferritin degradation, subsequently leading to the increase of lysOSomal iron that is utilized by ART for its cytotoxic effect on cancer cells.
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Andrographolide sensitizes cisplatin-induced apoptosis via suppression of autophagosome-lysosome fusion in human cancer cells.

TL;DR: It is suggested that Andro could be a promising anti-cancer agent in combination therapy via its potent inhibitory effect on autophagy by disrupting autophagosome-lysosome fusion.