title: The bioactive compounds alpha-chaconine and gallic acid in potato extracts decrease survival and induce apoptosis in LNCaP and PC3 prostate cancer cells.
abstract: We recently reported that colored potato extracts and an anthocyanin rich fraction suppressed lymph-node carcinoma of the prostate (LNCaP) and prostate cancer-3 (PC-3) prostate cancer cell proliferation and induced apoptosis via caspase-dependent and caspase-independent pathways. Chlorogenic acid, caffeic acid, gallic acid, catechin, malvidin, and glycoalkaloids (alpha-chaconine and solanine) have now been identified as the major bioactive components of potato, and their effects on LNCaP and PC-3 cell proliferation and apoptosis have been investigated. alpha-chaconine (5 microg/ml) and gallic acid (15 microg/ml) exhibited potent antiproliferative properties and increased cyclin-dependent kinase inhibitor p27 levels in both cell lines. Both alpha-chaconine and gallic acid induced poly [adenosine diphosphate (ADP)] ribose polymerase cleavage and caspase-dependent apoptosis in LNCaP cells; however, caspase-independent apoptosis through nuclear translocation of endonuclease G was observed in both LNCaP and PC-3 cells. alpha-chaconine and gallic acid activated c-Jun N-terminal protein kinase (JNK), and this response played a major role in induction of caspase-dependent apoptosis in LNCaP cells; whereas modulation of JNK and mitogen-activated protein kinase did not affect alpha-chaconine- and gallic acid-induced caspase-independent apoptosis. These results suggest that apoptosis induced by whole potato extracts in prostate cancer cell lines may be in part due to alpha-chaconine and gallic acid.
authors.affiliation: Colorado State University, Fort Collins, Colorado, USA.
authors.forename: Lavanya
authors.initials: L
authors.lastname: Reddivari
authors.forename: Jairam
authors.initials: J
authors.lastname: Vanamala
authors.forename: Stephen H
authors.initials: SH
authors.lastname: Safe
authors.forename: J Creighton
authors.initials: JC
authors.lastname: Miller
mesh_terms: D018949:Antigens, CD1 / Q000032:analysis; D017209:Apoptosis / Q000187:drug effects*; D020169:Caspases / Q000502:physiology; D045744:Cell Line, Tumor; D049109:Cell Proliferation / Q000187:drug effects; D050760:Cyclin-Dependent Kinase Inhibitor p27; D048049:Extracellular Signal-Regulated MAP Kinases / Q000378:metabolism; D005707:Gallic Acid / Q000494:pharmacology*; D006801:Humans; D047908:Intracellular Signaling Peptides and Proteins / Q000032:analysis; D048031:JNK Mitogen-Activated Protein Kinases / Q000378:metabolism; D008297:Male; D010936:Plant Extracts / Q000494:pharmacology*; D011471:Prostatic Neoplasms / Q000188:drug therapy* / Q000473:pathology; D012992:Solanine / Q000031:analogs & derivatives* / Q000494:pharmacology; D011198:Solanum tuberosum / Q000737:chemistry*
chemical_list: D018949:Antigens, CD1; C436291:CDKN1B protein, human; D047908:Intracellular Signaling Peptides and Proteins; D010936:Plant Extracts; D050760:Cyclin-Dependent Kinase Inhibitor p27; D012992:Solanine; C011860:alpha-chaconine; D005707:Gallic Acid; D048049:Extracellular Signal-Regulated MAP Kinases; D048031:JNK Mitogen-Activated Protein Kinases; D020169:Caspases