Non-apoptotic cell death in malignant tumor cells and natural compounds
Traditional cancer therapy is mainly targeting on enhancing cell apoptosis, however, it is well established that many cancer cells are chemo-resistant and defective in apoptosis induction. Therefore, it may have important therapeutic implications to exploit some novel natural compounds based on non-...
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Veröffentlicht in: | Cancer letters 2018-04, Vol.420, p.210-227 |
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Format: | Artikel |
Sprache: | eng |
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Zusammenfassung: | Traditional cancer therapy is mainly targeting on enhancing cell apoptosis, however, it is well established that many cancer cells are chemo-resistant and defective in apoptosis induction. Therefore, it may have important therapeutic implications to exploit some novel natural compounds based on non-apoptotic programmed cell death. Currently, accumulating evidence shows that the compounds from nature source can induce non-apoptotic programmed cell death in cancer cells, and therefore these natural compounds have gained a great promise for the future anticancer therapeutics. In this review, we will concentrate our efforts on the latest developments regarding major forms of non-apoptotic programmed cell death--autophagic cell death, necroptosis, ferroptosis, pyroptosis, glutamoptosis and exosome-associated cell death. Our increased understanding of the role of natural compounds in regulating non-apoptotic programmed cell death will hopefully provide prospective strategies for cancer therapy.
•It is well established that many cancer cells are chemo-resistant and defective in apoptosis induction.•It may have important therapeutic implications to exploit some novel natural compounds based on non-apoptotic programmed cell death.•The compounds from nature source can induce non-apoptotic programmed cell death in cancer cells.•Our increased understanding of the role of natural compounds in regulating non-apoptotic programmed cell death will hopefully provide prospective strategies for cancer therapy. |
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ISSN: | 0304-3835 1872-7980 |
DOI: | 10.1016/j.canlet.2018.01.061 |