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Vanadyl complexes discriminate between neuroblastoma cells and primary neurons by inducing cell-specific apoptotic pathways.

Abstract：

:Vanadium compounds have arisen as potential therapeutic agent for the treatment of cancers over the past decades. A few studies suggested that vanadyl complexes may discriminate between the cancerous and the normal cells. Here, we reported the investigation on the pro-apoptotic effect and the underlying mechanism of bis(acetylacetonato) oxovanadium(IV) ([VO(acac)2]) on SH-SY5Y neuroblastoma cells in comparison with that of mouse primary cortex neurons. The experimental results revealed that [VO(acac)2] showed about 10-fold higher cytotoxicity (IC50 ~16 μM) on the neuroblastoma cells than on normal neurons (IC50 ~250 μM). Further analysis indicated that the vanadyl complex suppressed the growth of neuroblastoma cells via different pathways depending on its concentration. It induced a special cyclin D-mediated and p53-independent cell apoptosis at <50 μM but cell cycle arrests at >50 μM. In contrast, [VO(acac)2] promoted cell viability of primary neurons in the concentration range of 0-150 μM; while [VO(acac)2] at hundreds of μM would cause neuronal death possibly via the reactive oxygen species (ROS)-mediated signal pathways. The extraordinary discrimination between neuroblastoma cells and primary neurons suggests potential application of vanadyl complexes for therapeutic treatment of neuroblastoma. In addition, the p53-independent apoptotic pathways induced by vanadyl complexes may provide new insights for future discovery of new anticancer drugs overcoming the chemo-resistance due to p53 mutation.

journal_name

J Inorg Biochem

journal_title

Journal of inorganic biochemistry

authors

Zhang Y,Wang L,Zeng K,Wang K,Yang X

doi

10.1016/j.jinorgbio.2018.08.005

subject

Has Abstract

pub_date

2018-11-01 00:00:00

pages

76-87

eissn

0162-0134

issn

1873-3344

pii

S0162-0134(18)30239-3

journal_volume

188

pub_type

杂志文章

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