Naringenin‐Induced Apoptotic Cell Death in Prostate Cancer Cells Is Mediated via the PI3K/AKT and MAPK Signaling Pathways

Whasun Lim; Fuller W. Bazer; Gwonhwa Song

doi:10.1002/jcb.25729

journal article Jan 10, 2017

Naringenin‐Induced Apoptotic Cell Death in Prostate Cancer Cells Is Mediated via the PI3K/AKT and MAPK Signaling Pathways

Whasun Lim

Fuller W. Bazer Gwonhwa Song

Journal of Cellular Biochemistry Vol. 118 No. 5 pp. 1118-1131 · Wiley

View at Publisher Save 10.1002/jcb.25729

Abstract

ABSTRACTProstate cancer is the most common cancer in men and the second most common cause of cancer‐related deaths in men. Although, various drugs targeting the androgen receptor are normally used, the patients frequently undergo recurrence of the disease. To overcome these limitations, natural compounds have been researched for evidence that they suppress progression and metastasis of various cancer cells. In the present study, we investigated effects of naringenin, a natural anti‐oxidant flavonoid derived from citrus, on prostate cancer cells (PC3 and LNCaP). Results of present study with PC3 and LNCaP cells revealed that naringenin inhibited proliferation and migration, while inducing apoptosis and ROS production by those cells. In addition, naringenin‐induced loss of mitochondrial membrane potential and increased Bax and decreased Bcl‐2 proteins in PC3 cells, but not LNCaP cells. In a dose‐dependent manner, naringenin decreased phosphorylation of ERK1/2, P70S6K, S6, and P38 in PC3 cells, and reduced phosphorylation of ERK1/2, P53, P38, and JNK proteins in LNCaP cells. However, naringenin activated phosphorylation of AKT in both PC3 and LNCaP cells. Then, targeted signaling proteins associated with viability of PC3 and LNCaP cells were analyzed using pharmacological inhibitors of AKT and ERK1/2 cell signaling pathways. Moreover, we compared the apoptotic effects of naringenin and paclitaxel alone and in combination to find that naringenin enhanced the efficiency of paclitaxel to suppress progression of prostate cancer cell lines. Collectively, these results indicate that naringenin is a potential chemotherapeutic agent for treatment of prostate cancer. J. Cell. Biochem. 118: 1118–1131, 2017. © 2016 Wiley Periodicals, Inc.

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References

Details

Published: Jan 10, 2017
Vol/Issue: 118(5)
Pages: 1118-1131
License: View

Authors

W

Whasun Lim

Department of Biotechnology and Institute of Animal Molecular Biotechnology College of Life Sciences and Biotechnology Korea University Seoul 02841 Republic of Korea

F

Fuller W. Bazer

Center for Animal Biotechnology and Genomics and Department of Animal Science Texas A&M University College Station 77843‐2471 Texas

G

Gwonhwa Song

Department of Biotechnology and Institute of Animal Molecular Biotechnology College of Life Sciences and Biotechnology Korea University Seoul 02841 Republic of Korea

Funding

Ministry of Education, Science and Technology Award: 2015R1D1A1A01059331

Cite This Article

Whasun Lim, Fuller W. Bazer, Gwonhwa Song (2017). Naringenin‐Induced Apoptotic Cell Death in Prostate Cancer Cells Is Mediated via the PI3K/AKT and MAPK Signaling Pathways. Journal of Cellular Biochemistry, 118(5), 1118-1131. https://doi.org/10.1002/jcb.25729

Naringenin‐Induced Apoptotic Cell Death in Prostate Cancer Cells Is Mediated via the PI3K/AKT and MAPK Signaling Pathways

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