Please use this identifier to cite or link to this item: https://scholarbank.nus.edu.sg/handle/10635/108678
Title: Progress in phytochemicals' induction of autophagic cell death in cancer cells and regulation of nuclear receptors
Authors: Xu, Y.-Y.
Shen, H.-M. 
Zhu, X.-Q.
Keywords: Autophagy
Neoplasms
Phytochemicals
Receptors, nuclear
Issue Date: Apr-2008
Citation: Xu, Y.-Y.,Shen, H.-M.,Zhu, X.-Q. (2008-04). Progress in phytochemicals' induction of autophagic cell death in cancer cells and regulation of nuclear receptors. Chinese Journal of Pharmacology and Toxicology 22 (2) : 151-155. ScholarBank@NUS Repository.
Abstract: Autophagic cell death is a kind of caspase-independent programmed cell death. Nuclear receptors can regulate transcription and translation of the downstream genes, affect expressions of autophagy-related genes, and regulate autophagy in cancer cells. It was found that many phytochemicals, including isothiocyanate, flavonoid, saponin, phytoestrogen, anthraquinones and alkaloid, can induce autophagic cell death in cancer cells. Nuclear receptors can be combined with and activated by phytochemicals, comprising isothiocyanate, flavonoid and phytoestrogen. Some drugs, which exert their functions through directly interacting with nuclear receptors, such as tamoxifen, 15-deoxy Δ12,14-prostaglandin J2, EB1089, sesquiterpene analogs of paclitaxel AGS 115 and EFDAC, induce autophagic cell death in special cancer. All this information provides a clue to the relationship among phytochemicals, nuclear receptors and autophagy.
Source Title: Chinese Journal of Pharmacology and Toxicology
URI: http://scholarbank.nus.edu.sg/handle/10635/108678
ISSN: 10003002
Appears in Collections:Staff Publications

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