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Updated: Mar 8, 2026
An Orthotopic Murine Model of Human Prostate Cancer Metastasis
Published on: September 18, 2013
Liver X receptor activation inhibits PC-3 prostate cancer cells via the beta-catenin pathway
Kuang Youlin1, Zhang Li2, He Weiyang1
1Department of Urology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China.
Background:
Liver X receptors (LXRs) are nuclear receptors family of ligand-dependent transcription factors that play a crucial role in regulating cholesterol metabolism and inflammation. Recent studies show that LXR agonists exhibit anti-cancer activities in a variety of cancer cell lines including prostate. To further identify the potential mechanisms of LXRα activation on prostate cancer, we investigated the effect of LXR agonist T0901317 on PC3 prostate cancer cell and in which activity of beta-catenin pathway involved.
Methods:
Prostate cancer PC3 cells were transfected with LXR-a siRNA and treated with LXR activator T0901317. qRT-PCR and western blot were used to detect the LXR-a expression. beta-catenin, cyclin D1 and c-MYC were analyzed by western blot. Cell apoptosis was examined by flow cytometry and Cell proliferation was assessed by Cell Counting Kit-8 assay. Cell migration was detected by Transwell chambers.
Results:
Data showed that T0901317 significantly inhibited PC3 cell proliferation as well as invasion and increased apoptosis in vitro. Furthermore, we found that LXRα activation induced the reduction of beta-catenin expression in PC3 cells, and this inhibitory effect could be totally abolished when cells were treated with LXRα. Meanwhile, the expression of beta-catenin target gene cyclin D1 and c-MYC were also decreased.
Conclusions:
This study provided additional evidence that LXR activation inhibited PC-3 prostate cancer cells via suppressing beta-catenin pathway.
Insights
Liver X receptor (LXR) activation inhibits prostate cancer cell growth by decreasing beta-catenin pathway activity. This LXR agonist treatment reduced cell proliferation and invasion while increasing apoptosis in PC3 cells.
Area of Science:
- Molecular Biology
- Cancer Research
- Pharmacology
Background:
- Liver X receptors (LXRs) are nuclear receptors regulating cholesterol and inflammation.
- LXR agonists show anti-cancer effects, particularly in prostate cancer.
- Investigating LXRα activation mechanisms in prostate cancer is crucial.
Purpose of the Study:
- To determine the effect of LXR agonist T0901317 on PC3 prostate cancer cells.
- To elucidate the role of the beta-catenin pathway in LXRα-mediated anti-cancer activity.
Main Methods:
- PC3 cells were treated with T0901317 and LXRα siRNA.
- Gene and protein expression (LXRα, beta-catenin, cyclin D1, c-MYC) analyzed by qRT-PCR and Western blot.
- Cell proliferation, apoptosis, and migration assessed using CCK-8, flow cytometry, and Transwell assays.
Main Results:
- T0901317 significantly inhibited PC3 cell proliferation, invasion, and increased apoptosis.
- LXRα activation reduced beta-catenin expression, which was reversed by LXRα siRNA.
- Expression of beta-catenin target genes cyclin D1 and c-MYC also decreased.
Conclusions:
- LXR activation suppresses PC-3 prostate cancer cell proliferation and invasion.
- The beta-catenin pathway is a key mediator of LXR's anti-cancer effects in prostate cancer.
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