Plumbagin induces G2-M arrest and autophagy by inhibiting the AKT/mammalian target of rapamycin pathway in breast cancer cells

This study is the first to investigate the anticancer effect of plumbagin in human breast cancer cells. Plumbagin exhibited cell proliferation inhibition by inducing cells to undergo G 2 -M arrest and autophagic cell death. Blockade of the cell cycle was associated with increased p21/WAF1 expression...

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Veröffentlicht in:	Molecular cancer therapeutics 2006-12, Vol.5 (12), p.3209-3221
Hauptverfasser:	Kuo, Po-Lin, Hsu, Ya-Ling, Cho, Chien-Yu
Format:	Artikel
Sprache:	eng
Schlagworte:	AKT Animals Antineoplastic Agents, Phytogenic - pharmacology Apoptosis - drug effects autophagy Autophagy - drug effects Breast Neoplasms - drug therapy Breast Neoplasms - genetics Breast Neoplasms - metabolism Breast Neoplasms - pathology cell cycle Cell Division - drug effects Cell Growth Processes - drug effects Cell Line, Tumor Female G2 Phase - drug effects Humans Mice Mice, Inbred BALB C Mice, Nude mTOR Naphthoquinones - pharmacology Phosphatidylinositol 3-Kinases - antagonists & inhibitors Phosphatidylinositol 3-Kinases - metabolism plumbagin Protein Kinases - metabolism Proto-Oncogene Proteins c-akt - antagonists & inhibitors Proto-Oncogene Proteins c-akt - genetics Proto-Oncogene Proteins c-akt - metabolism RNA, Small Interfering - genetics Sirolimus - immunology TOR Serine-Threonine Kinases
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