title: D-pinitol promotes apoptosis in MCF-7 cells via induction of p53 and Bax and inhibition of Bcl-2 and NF-κB.
abstract: Development of drugs from natural products has been undergoing a gradual evoluation. Many plant derived compounds have excellent therapeutic potential against various human ailments. They are important sources especially for anticancer agents. A number of promising new agents are in clinical development based on their selective molecular targets in the field of oncology. D-pinitol is a naturally occurring compound derived from soy which has significant pharmacological activitites. Therefore we selected D-pinitol in order to evaluate apoptotic potential in the MCF-7 cell line. Human breast cancer cells were treated with different concentrations of D-pinitol and cytotoxicity was measured by MTT and LDH assays. The mechanism of apoptosis was studied with reference to expression of p53, Bcl-2, Bax and NF-kB proteins. The results revealed that D-pinitol significantly inhibited the proliferation of MCF-7 cells in a concentration-dependent manner, while upregulating the expression of p53, Bax and down regulating Bcl-2 and NF-kB. Thus the results obtained in this study clearly vindicated that D-pinitol induces apotosis in MCF-7 cells through regulation of proteins of pro- and anti-apoptotic cascades.
authors.affiliation: Department of Pharmacology and Environmental Toxicology, Dr. ALM PG Institute of Basic Medical Sciences, University of Madras, Chennai, India E-mail : balumppet@gmail.com.
authors.forename: Thamaraiselvan
authors.initials: T
authors.lastname: Rengarajan
authors.forename: Natarajan
authors.initials: N
authors.lastname: Nandakumar
authors.forename: Peramaiyan
authors.initials: P
authors.lastname: Rajendran
authors.forename: Lingaiah
authors.initials: L
authors.lastname: Haribabu
authors.forename: Ikuo
authors.initials: I
authors.lastname: Nishigaki
authors.forename: Maruthaiveeran Periyasamy
authors.initials: MP
authors.lastname: Balasubramanian
mesh_terms: D000970:Antineoplastic Agents / Q000494:pharmacology; D017209:Apoptosis / Q000187:drug effects*; D001943:Breast Neoplasms / Q000188:drug therapy* / Q000473:pathology; D045744:Cell Line, Tumor; D049109:Cell Proliferation / Q000187:drug effects; D002470:Cell Survival / Q000187:drug effects; D053938:DNA Fragmentation / Q000187:drug effects; D005260:Female; D015972:Gene Expression Regulation, Neoplastic; D005978:Glutathione / Q000096:biosynthesis; D006801:Humans; D007294:Inositol / Q000031:analogs & derivatives* / Q000494:pharmacology; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D061986:MCF-7 Cells; D028321:Plant Preparations / Q000494:pharmacology; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000096:biosynthesis; D013025:Glycine max / Q000378:metabolism; D051996:Transcription Factor RelA / Q000096:biosynthesis / Q000378:metabolism; D016159:Tumor Suppressor Protein p53 / Q000096:biosynthesis*; D051028:bcl-2-Associated X Protein / Q000096:biosynthesis*
chemical_list: D000970:Antineoplastic Agents; D028321:Plant Preparations; D019253:Proto-Oncogene Proteins c-bcl-2; D051996:Transcription Factor RelA; D016159:Tumor Suppressor Protein p53; D051028:bcl-2-Associated X Protein; C021730:pinitol; D007294:Inositol; D007770:L-Lactate Dehydrogenase; D005978:Glutathione