title: ProstaCaid inhibits tumor growth in a xenograft model of human prostate cancer.
abstract: We have recently demonstrated that the dietary supplement ProstaCaid (PC) inhibits growth and invasive behavior of PC-3 human prostate cancer cells in vitro. In the present study, we evaluated toxicity and whether PC suppresses growth of prostate cancer in a xenograft model of human prostate cancer cells implanted in mice. Here, we show that an oral administration of PC (100, 200 and 400 mg/kg) did not affect body weight or activity of liver enzymes (ALT, AST) and did not show any sign of toxicity in liver, spleen, kidney, lung and heart tissues in mice. In addition, PC treatment resulted in the inhibition of tumor volumes (1024.6 ± 378.6 vs. 749.3 ± 234.3, P<0.001) in a xenograft model of prostate cancer with human hormone refractory (independent) PC-3 prostate cancer cells. Moreover, qRT-PCR analysis demonstrated significant upregulation of expression of CDKN1A (p21) and inhibition of expression of IGF2, NR2F2 and PLAU (uPA) genes by an oral administration of PC in prostate cancer xenografts. Our study demonstrates that the concentrations of the dietary supplement ProstaCaid tested did not show signs of toxicity, and its oral application has significant anticancer activity in vivo and can be considered as an alternative treatment for prostate cancer patients.
authors.affiliation: Cancer Research Laboratory, Methodist Research Institute, Indiana                     University Health, Indianapolis, IN, USA.
authors.forename: Jiahua
authors.initials: J
authors.lastname: Jiang
authors.forename: Jagadish
authors.initials: J
authors.lastname: Loganathan
authors.forename: Isaac
authors.initials: I
authors.lastname: Eliaz
authors.forename: Colin
authors.initials: C
authors.lastname: Terry
authors.forename: George E
authors.initials: GE
authors.lastname: Sandusky
authors.forename: Daniel
authors.initials: D
authors.lastname: Sliva
mesh_terms: D000284:Administration, Oral; D000818:Animals; D000970:Antineoplastic Agents / Q000008:administration & dosage / Q000494:pharmacology* / Q000633:toxicity; D051837:COUP Transcription Factor II / Q000235:genetics; D045744:Cell Line, Tumor; D050759:Cyclin-Dependent Kinase Inhibitor p21 / Q000235:genetics; D019587:Dietary Supplements; D015972:Gene Expression Regulation, Neoplastic / Q000187:drug effects; D006801:Humans; D007335:Insulin-Like Growth Factor II / Q000235:genetics; D008297:Male; D051379:Mice; D008819:Mice, Nude; D010936:Plant Extracts / Q000008:administration & dosage / Q000494:pharmacology* / Q000633:toxicity; D011471:Prostatic Neoplasms / Q000188:drug therapy* / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D060888:Real-Time Polymerase Chain Reaction; D015398:Signal Transduction / Q000187:drug effects; D013997:Time Factors; D047368:Tumor Burden / Q000187:drug effects*; D014568:Urokinase-Type Plasminogen Activator / Q000235:genetics; D023041:Xenograft Model Antitumor Assays
chemical_list: D000970:Antineoplastic Agents; D051837:COUP Transcription Factor II; D050759:Cyclin-Dependent Kinase Inhibitor p21; D007335:Insulin-Like Growth Factor II; D010936:Plant Extracts; D014568:Urokinase-Type Plasminogen Activator; C493956:CDKN1A protein, human; C035170:IGF2 protein, human; C573121:ProstaCaid; C095569:NR2F2 protein, human