A bismuth diethyldithiocarbamate compound promotes apoptosis in HepG2 carcinoma, cell cycle arrest and inhibits cell invasion through modulation of the NF-κB activation pathway

The compound with R=CH2CH3 in Bi(S2CNR2)3 (1) is highly cytotoxic against a range of human carcinoma, whereas that with R=CH2CH2OH (2) is considerably less so. Both 1 and 2 induce apoptosis in HepG2 cells with some evidence for necrosis induced by 2. Based on DNA fragmentation, caspase activities an...

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Bibliographic Details
Published in:	Journal of inorganic biochemistry 2014-01, Vol.130, p.38-51
Main Authors:	Ishak, Dayang Hazwani Abang, Ooi, Kah Kooi, Ang, Kok-Pian, Akim, Abdah Md, Cheah, Yoke-Kqueen, Nordin, Norshariza, Halim, Siti Nadiah Binti Abdul, Seng, Hoi-Ling, Tiekink, Edward R.T.
Format:	Article
Language:	English
Subjects:	Antineoplastic Agents - chemistry Antineoplastic Agents - pharmacology Apoptosis Apoptosis - drug effects Apoptosis - genetics Bismuth Bismuth - chemistry Cell cycle Cell Cycle Checkpoints - drug effects Cell Membrane Permeability - drug effects Cell Movement - drug effects Death-Associated Protein Kinases - genetics Drug Screening Assays, Antitumor - methods Gene Expression Regulation - drug effects Hep G2 Cells - drug effects Humans Metallopharmaceuticals NF-kappa B - metabolism NF-κB Organometallic Compounds - chemistry Organometallic Compounds - pharmacology Signal Transduction - drug effects X-Linked Inhibitor of Apoptosis Protein - genetics X-Linked Inhibitor of Apoptosis Protein - metabolism
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