J Cancer Prev 2020; 25(2): 87-99
Published online June 30, 2020
https://doi.org/10.15430/JCP.2020.25.2.87
© Korean Society of Cancer Prevention
Larissa Akemi Kido1,2 , Eun-Ryeong Hahm3 , Su-Hyeong Kim3 , Andressa Mara Baseggio1 , Valeria Helena Alves Cagnon2 , Shivendra V. Singh3,4,* , Mário Roberto Maróstica Jr.1,*
1Department of Food and Nutrition, Faculty of Food Engineering, University of Campinas, 2Department of Structural and Functional Biology, Institute of Biology, University of Campinas, Campinas, Brazil, 3Department of Pharmacology and Chemical Biology and 4UPMC Hillman Cancer Center, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA
Correspondence to :
Mário Roberto Maróstica Jr., E-mail: mmarosti@unicamp.br, https://orcid.org/0000-0001-8877-3160
Shivendra V. Singh, E-mail: singhs@upmc.edu, https://orcid.org/0000-0002-3733-144X
*These authors contributed equally to this work as co-correspondence authors
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
Piceatannol (PIC), a polyphenol presents in many vegetables and fruits including yellow passion fruit extract (PFE; Passiflora edulis), has anti-cancer activity, but its molecular targets are still poorly understood. The aims of this study were to investigate the molecular mechanistic actions of PIC in prostate cancer cell lines and to test if the extract from PFE rich in PIC can affect the growth of prostate cancer cells in the Transgenic Adenocarcinoma of the Mouse Prostate (TRAMP) model. The PC-3, 22Rv1, LNCaP, and VCaP prostate cancer cells were exposed to PIC (10-40 μM), and cell viability, lactate measurement, Western blot, and flow cytometric analyses were performed. For an in vivo experiments, eight-week-old TRAMP mice (n = 10 per group each) received an aqueous extract of PFE containing 20 mg of PIC/kg or water (control group) by gavage for 4 or 10 weeks for further analyses. PIC treatment concentration- and time-dependently reduced viability of all cell lines tested. 22Rv1 and LNCaP cells treated with PIC did not exhibit any significant alteration in the intracellular accumulation of lactate. PIC treatment caused G0/G1 phase cell cycle arrest and induction of apoptosis in both LNCaP and 22Rv1 cells. PIC-treated cells exhibited altered protein levels of p53, p21, cyclin D1, and cyclin-dependent kinase 4 (cdk4). The short and long-term PFE treatments also affected p21, cyclin D1 and cdk4 and delayed disease progression in TRAMP, with a decreased incidence of preneoplastic lesions. In conclusion, PIC apparently does not alter glucose metabolism in prostate cancer cells, while cell cycle arrest and p53 modulation are likely important in anti-cancer effects of PIC alone or as a food matrix byproduct in prostate cancer cells, especially those with an androgen-dependent phenotype.
Keywords: Prostate cancer, Bioactive compounds, Passion fruit, Piceatannol, Transgenic adenocarcinoma of the mouse prostate
Kader Turkekul, Suat Erdogan
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