NDLI: Detailed analysis of pro-apoptotic signaling and metabolic adaptation triggered by a N-heterocyclic carbene

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Metallomics Vol - 6 Issue - 8

Metallomics Vol - 6 Issue - 7

Metallomics Vol - 6 Issue - 6

Metallomics Vol - 6 Issue - 5

Metallomics Vol - 6 Issue - 4

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Metallomics Vol - 6 Issue - 2

Detailed analysis of pro-apoptotic signaling and metabolic adaptation triggered by a N-heterocyclic carbene–gold(i) complex

Content Provider	Royal Society of Chemistry (RSC)
Author	Rubbiani, Riccardo Alborzinia, Hamed Ott, Ingo Jünger, Anja Holenya, Pavlo Can, Suzan Cheng, Xinlai Wölfl, Stefan
Copyright Year	2014
Abstract	Due to their broad spectrum of biological activity and antiproliferative effect on different human cancer cell lines, gold compounds have been in the focus of drug research for many years. Gold(I)–N-heterocyclic carbene complexes are of particular interest, because of their stability, ease of derivatization and clear cytotoxicity in cancer cells. To obtain a more detailed view of the molecular mechanisms underlying their cellular activity, we used a novel gold(I)–N-heterocyclic carbene complex, [triphenylphosphane-(1,3-diethyl-5-methoxy-benzylimidazol-2-ylidene)]gold(I) iodide and investigated changes in cellular signaling pathways using quantitative signal transduction protein microarray analysis. We also analyzed changes in cell metabolism in a time-dependent manner by on-line metabolic measurements and used isolated mitochondria to elucidate the direct effects on this cell organelle. We found strong cytotoxic effects in cancer cells, accompanied by an immediate and irreversible loss of mitochondrial respiration as well as by a crucial imbalance of the intracellular redox state, resulting in apoptotic cell death. ELISA microarray analysis of signal transduction pathways revealed a time-dependent up-regulation of pro-apoptotic signaling proteins, e.g. p38 and JNK, whereas pro-survival signals that are directly linked to the thioredoxin system were down-regulated, which pinpoints to thioredoxin reductase as a central target of the compound. Further results suggest that DNA is an indirect target of the compound. Based on our findings, we outline a signaling model for the molecular mechanism underlying the antiproliferative activity of the gold(I)–N-heterocyclic carbene complex investigated, which provides a good general model for the known pattern of cell death induced by this class of substances.
Starting Page	1591
Ending Page	1601
Page Count	11
File Format	HTM / HTML PDF
ISSN	17565901
Volume Number	6
Issue Number	9
Journal	Metallomics
DOI	10.1039/c4mt00075g
Language	English
Publisher	Royal Society of Chemistry
Access Restriction	Open
Subject Keyword	Persistent carbene Redox Cytotoxicity Protein microarray Metabolism Microarray Thioredoxin Thioredoxin reductase Mitochondrion Signal transduction P38 mitogen-activated protein kinases DNA Cellular respiration Organelle C-Jun N-terminal kinases ELISA Cancer Iodine
Content Type	Text
Resource Type	Article
Subject	Chemistry Medicine Metals and Alloys Biochemistry Biomaterials Biophysics

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Detailed analysis of pro-apoptotic signaling and metabolic adaptation triggered by a N-heterocyclic carbene–gold(i) complex

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