Next Article in Journal
Pelargonium endlicherianum Fenzl. Root Extract Suppresses Cell Proliferation of Prostate Cancer Cells
Previous Article in Journal
Cyclodextrine Based Nanogels and Phase Solubility Studies of Flurbiprofen as a Chemopreventive Agent
Article Menu

Article Versions

Export Article

Open AccessAbstract
Proceedings 2017, 1(10), 992; doi:10.3390/proceedings1100992

Celastrol Modulates Lipid Synthesis via PI3K/Akt/mTOR Signaling Axis to finalize Cell Death Response in Prostate Cancer Cells

Atakoy Campus, Department of Molecular Biology and Genetics, Istanbul Kultur University, Istanbul 34156, Turkey
Presented at the 2nd International Conference on Natural Products for Cancer Prevention and Therapy, Kayseri, Turkey, 8–11 November 2017.
*
Author to whom correspondence should be addressed.
Published: 15 November 2017
Download PDF [154 KB, uploaded 15 November 2017]

Abstract

FASN is key enzyme during lipid biogenesis is associated with prostate cancer. In this study, we aim to investigate the potential role of celastrol, root extracts of Tripterygium wilfordii on modulation of lipid biosynthesis-associated PI3K/Akt signaling. To determine the effect of celastrol on cell viability, prostate cancer cells were exposed with celastrol in dose dependent manner. AR (+) LNCaP and AR (−) DU145 and PC3 cell viability were inhibited by celastrol with IC50 in the range of 0.05–1 µM. To address the role of celastrol on cell death mechanism, celastrol-treated prostate cancer cells were evaluated with immunoblotting and flow cytometric analysis. Celastrol significantly upregulated PARP and caspase 9 cleavage also increased sub-G1 population. Celastrol also inhibited cell migration and invasion. These effects were associated with decreased PI3K/Akt signaling axis and downregulation of epithelial mesenchymal transition in prostate cancer cells. Likewise, lipid biosynthesis was downregulated with celastrol, however inhibition of PI3K/Akt signaling axis via LY294002 further decrease the cell migration and proliferation rate in prostate cancer cells. Our data suggest that, celastrol suppressed cell proliferation via inhibition of lipid biosynthesis through downregulation of PI3K/Akt signal axis. Targeting lipid metabolism-related enzymes in prostate cancer may offer new avenues for therapeutic approaches.
Keywords: celastrol; FASN; prostate cancer celastrol; FASN; prostate cancer
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

Scifeed alert for new publications

Never miss any articles matching your research from any publisher
  • Get alerts for new papers matching your research
  • Find out the new papers from selected authors
  • Updated daily for 49'000+ journals and 6000+ publishers
  • Define your Scifeed now

SciFeed Share & Cite This Article

MDPI and ACS Style

Arisan, E.D.; Rencüzoğulları, Ö.; Çoker-Gürkan, A.; Obakan-Yerlikaya, P.; Palavan-Ünsal, N. Celastrol Modulates Lipid Synthesis via PI3K/Akt/mTOR Signaling Axis to finalize Cell Death Response in Prostate Cancer Cells. Proceedings 2017, 1, 992.

Show more citation formats Show less citations formats

Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Article Metrics

Article Access Statistics

1

Comments

[Return to top]
Proceedings EISSN 2504-3900 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top