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Biochem Pharmacol. 2015 Mar 1;94(1):1-11. doi: 10.1016/j.bcp.2014.12.018. Epub 2015 Jan 3.

Cancer-type-specific crosstalk between autophagy, necroptosis and apoptosis as a pharmacological target.

Author information

1
Laboratoire de Biologie Moléculaire et Cellulaire du Cancer, Hôpital Kirchberg, 9, rue Edward Steichen, L-2540 Luxembourg, Luxembourg.
2
College of Pharmacy, Seoul National University, 1 Gwanak-ro, Gwanak-gu, Seoul 151-742, Republic of Korea. Electronic address: marc.diederich@lbmcc.lu.

Abstract

Cell death plays an essential role in the development of organs, homeostasis, and cancer. Apoptosis and programmed necrosis are two major types of cell death, characterized by different cell morphology and pathways. Accumulating evidence shows autophagy as a new alternative target to treat tumor resistance. Besides its well-known pro-survival role, autophagy can be a physiological cell death process linking apoptosis and programmed necrosis cell death pathways, by various molecular mediators. Here, we summarize the effects of pharmacologically active compounds as modulators of different types of cancer cell death depending on the cellular context. Indeed, current findings show that both natural and synthetic compounds regulate the interplay between apoptosis, autophagy and necroptosis stimulating common molecular mediators and sharing common organelles. In response to specific stimuli, the same death signal can cause cells to switch from one cell death modality to another depending on the cellular setting. The discovery of important interconnections between the different cell death mediators and signaling pathways, regulated by pharmacologically active compounds, presents novel opportunities for the targeted treatment of cancer. The aim of this review is to highlight the potential role of these compounds for context-specific anticancer therapy.

KEYWORDS:

Anti-cancer therapy; Apoptosis; Autophagy; Cancer; Chemoprevention; Necroptosis; Personalized treatment

PMID:
25562745
DOI:
10.1016/j.bcp.2014.12.018
[Indexed for MEDLINE]

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