Institute Seminar Wednesday October 12th

Anders Bjartell

A. Bjartell
A. Bjartell
The institute seminar on Wednesday October 12th is given by Anders Bjartell from Department of Clinical Sciences and Department of Urology at Skåne University Hospital, Malmö, Sweden. Title of his talk:
Galiellalactone inhibits stem cell-like ALDH-positive prostate cancer cells
The seminar takes place in the Auditorium (Research Building Montebello) and starts at 12:00.
Anders Bjartell is Professor in Clinical Urology at the Department of Clinical Sciences, Division of Urological Cancers in Malmö, Lund University and Consultant and head of the clinical trial unit at the Department of Urology, University Hospital Skåne, Sweden. He was visiting investigator at the Department of Surgery at Memorial Sloan-Kettering Cancer Center) MSKCC from August 2005 until July 2007. He is responsible for biobanking of serum, urine and tissue samples from patients with prostate cancer in Malmö, Sweden and for collecting and organizing clinical data for several studies including EU-projects. He has an M.D. (1986) and a Ph.D. (1990) from Lund University, Sweden and a European exam for Urologists; F.E.B.U. (Fellow of the European Board of Urology) 2000. He has published more than 140 original articles in peer-reviewed journals. He has been an Associate Editor for European Urology since 2005 and President of the European Society for Urological Research (ESUR) since 2008.

Abstract:

Galiellalactone inhibits stem cell-like ALDH-positive prostate cancer cells

Anders Bjartell, Department of Clinical Sciences and Department of Urology, Skåne University Hospital, Malmö, Sweden

Galiellalactone is a potent and specific inhibitor of STAT3 signaling which has been shown to possess growth inhibitory effects on prostate cancer cells expressing active STAT3. In this study we aimed to investigate the effect of galiellalactone on prostate cancer stem cell-like cells. We explored the expression of aldehyde dehydrogenase (ALDH) as a marker for cancer stem cell-like cells in different human prostate cancer cell lines and the effects of galiellalactone on ALDH expressing (ALDH+) prostate cancer cells. ALDH+ subpopulations were detected and isolated from the human prostate cancer cell lines DU145 and long-term IL-6 stimulated LNCaP cells using ALDEFLUORH assay and flow cytometry. In contrast to ALDH2 cells, ALDH+ prostate cancer cells showed cancer stem cell-like characteristics such as increased self-renewing and colony forming capacity and tumorigenicity. In addition, ALDH+ cells showed an increased expression of putative prostate cancer stem cell markers (CD44 and integrin a2b1). Furthermore, ALDH+ cells expressed phosphorylated STAT3. Galiellalactone treatment decreased the proportion of ALDH+ prostate cancer cells and induced apoptosis of ALDH+ cells. The gene expression of ALDH1A1 was downregulated in vivo in galiellalactone treated DU145 xenografts. These findings emphasize that targeting the STAT3 pathway in prostate cancer cells, including prostate cancer stem cell-like cells, is a promising therapeutic approach and that galiellalactone is an interesting compound for the development of future prostate cancer drugs.

Speaker invited by Kristin Taskén, Tumor Biology