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Biological Activity of Molybdenum(II) Allyl Dicarbonyl Complexes with N–N Coligands of Variable Aromatic Surface Area on Adherent and Non‐adherent Human Cancer Cells
Author(s) -
Pfeiffer Hendrik,
Dragoun Maxim,
Prokop Aram,
Schatzschneider Ulrich
Publication year - 2013
Publication title -
zeitschrift für anorganische und allgemeine chemie
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.354
H-Index - 66
eISSN - 1521-3749
pISSN - 0044-2313
DOI - 10.1002/zaac.201300055
Subject(s) - apoptosis , denticity , chemistry , ligand (biochemistry) , stereochemistry , cell culture , programmed cell death , partition coefficient , cell growth , chelation , reagent , metal , biochemistry , biology , organic chemistry , receptor , genetics
A series of seven molybdenum(II) allyl dicarbonyl complexes of the general formula [Mo(allyl)(CO) 2 ( N ‐N)(py)] + , in which N‐N is a bidentate chelating polypyridyl ligand with variable aromatic surface area, was synthesized by a new two‐step approach and fully characterized by IR and NMR spectropscopy, ESI mass spectrometry, and elemental analysis. The n ‐octanol/water partition coefficient log P increased with the size of the N‐N ligand from –0.4 to +1.8. The biological activity on adherent HT‐29 and MCF‐7 as well as non‐adherent NALM‐6 human cancer cell lines was studied with various assays, allowing also an insight in the mechanism of cell death. Most of the title compounds showed high antiproliferative activity in the low micromolar concentration range on all three cell lines tested, which however did not correlate much with the log P values determined. Apoptosis could be demonstrated as the major pathway of cell death for selected compounds and cell lines, setting on at 5 μM for the most active complex. Interestingly, no difference in apoptosis induction was observed between MCF(+/–) cell lines differentiated by expression of pro‐apoptotic enzyme caspase‐3 (+) or a lack thereof (–). This indicates an apoptosis induction pathway, which is independent of caspase‐3.