Resveratrol enhances prostate cancer cell response to ionizing radiation. Modulation of the AMPK, Akt and mTOR pathways View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2011-12

AUTHORS

Ayesha Rashid, Caiqiong Liu, Toran Sanli, Evangelia Tsiani, Gurmit Singh, Robert G Bristow, Ian Dayes, Himu Lukka, James Wright, Theodoros Tsakiridis

ABSTRACT

BACKGROUND: Prostate cancer (PrCa) displays resistance to radiotherapy (RT) and requires radiotherapy dose escalation which is associated with greater toxicity. This highlights a need to develop radiation sensitizers to improve the efficacy of RT in PrCa. Ionizing radiation (IR) stimulates pathways of IR-resistance and survival mediated by the protein kinase Akt but it also activates the metabolic energy sensor and tumor suppressor AMP-Activated Protein Kinase (AMPK). Here, we examined the effects of the polyphenol resveratrol (RSV) on the IR-induced inhibition of cell survival, modulation of cell cycle and molecular responses in PrCa cells. METHODS: Androgen-insensitive (PC3), sensitive (22RV1) PrCa and PNT1A normal prostate epithelial cells were treated with RSV alone (2.5-10 μM) or in combination with IR (2-8 Gy). Clonogenic assays, cell cycle analysis, microscopy and immunoblotting were performed to assess survival, cell cycle progression and molecular responses. RESULTS: RSV (2.5-5 μM) inhibited clonogenic survival of PC3 and 22RV1 cells but not of normal prostate PNT1A cells. RSV specifically sensitized PrCa cells to IR, induced cell cycle arrest at G1-S phase and enhanced IR-induced nuclear aberrations and apoptosis. RSV enhanced IR-induced expression of DNA damage (γH2Ax) and apoptosis (cleaved-caspase 3) markers as well as of the cell cycle regulators p53, p21(cip1) and p27(kip1). RSV enhanced IR-activation of ATM and AMPK but inhibited basal and IR-induced phosphorylation of Akt. CONCLUSIONS: Our results suggest that RSV arrests cell cycle, promotes apoptosis and sensitizes PrCa cells to IR likely through a desirable dual action to activate the ATM-AMPK-p53-p21(cip1)/p27(kip1) and inhibit the Akt signalling pathways. More... »

PAGES

144

References to SciGraph publications

Identifiers

URI

http://scigraph.springernature.com/pub.10.1186/1748-717x-6-144

DOI

http://dx.doi.org/10.1186/1748-717x-6-144

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1041788809

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/22029423


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