期刊
BIOTECHNOLOGY ADVANCES
卷 32, 期 6, 页码 1111-1122出版社
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.biotechadv.2014.03.006
关键词
Apoptosis; Necrosis; Autophagy; Reactive oxygen species
资金
- Action Lions Vaincre le Cancer
- Televie Luxembourg
- Recherche Cancer et Sang foundation
- Recherches Scientifiques Luxembourg association
- Een Haerz fir kriibskrank Kanner association
- Action Lions Vaincre le Cancer association
- National Research Foundation of Korea (NRF) - Korea government, Ministry of Science, ICT & Future Planning (MSIP) [2011-0030001]
- National Research Foundation of Korea [2011-0030001] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
Cell death is an important physiological regulator during development, tissue homeostasis and stress response but it is also a protective tumor suppressive mechanism. Tumor cells almost universally acquire the ability to evade cell death pathways that in normal cells act as a protective mechanism to remove damaged cells. As a result a population of death-resistant cells with accumulating genetic and epigenetic abnormalities contributes to malignant transformation. Any alteration of the homeostatic balance between survival and death is therefore a critical factor in carcinogenesis. Several forms of cell death exist and cross talk among them is emerging; however, we still miss many molecular details. It becomes essential to revisit the role of each type of cell death to understand interconnections existing between different cell death pathways as well as the network of their mediators to eventually develop new effective strategies to kill cancer cells. More specifically, new therapies based on compounds selectively triggering apoptosis, necrosis or autophagy recently became both appealing and challenging. Despite the rather clear classification of the different cell death modalities according to morphological criteria and the attempt to describe them with distinct signaling pathways, the reality reveals a complex interplay between apoptosis, regulated necrosis and autophagy involving a heterogeneous mix of molecular mediators. Nature, presenting an almost endless plenitude of bioactive scaffolds, can efficiently contribute compounds that allow deciphering the intricate pathways of cell death pathways and thus eventually contribute to selectively target cancer-type specific pathways in an attempt to personalize cancer patient treatment depending on cancer death pathway specificities. The aim of this review is to provide first an overview of molecular cell death specificities and to highlight how compounds of natural origins, with or without hemisynthetic modifications, target unique thanatotic molecular constellations. (C) 2014 Elsevier Inc. All rights reserved.
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