Oops, you're using an old version of your browser so some of the features on this page may not be displaying properly.

MINIMAL Requirements: Google Chrome 24+Mozilla Firefox 20+Internet Explorer 11Opera 15–18Apple Safari 7SeaMonkey 2.15-2.23

Poster Display session 3

3839 - Fenofibrate impairs pro-tumorigenic potential of cancer stem cell-like cells within drug-resistant prostate cancer cell populations.


30 Sep 2019


Poster Display session 3


Translational Research

Tumour Site

Prostate Cancer


Tomasz Wróbel


Annals of Oncology (2019) 30 (suppl_5): v760-v796. 10.1093/annonc/mdz268


T. Wróbel, E. Karnas, J. Catapano, M. Luty, K. Piwowarczyk, E. Zuba-Surma, D. Ryszawy, J. Czyż

Author affiliations

  • Faculty Of Biochemistry, Biophysics And Biotechnology, Jagiellonian University, 30-387 - Krakow/PL


Login to access the resources on OncologyPRO.

If you do not have an ESMO account, please create one for free.

Abstract 3839


Multipotent cancer stem cells (CSC) are involved in micro-evolutionary tumor adaptation to therapeutic regimens. Due to their drug-resistance, they represent a promising target for treatment strategies of advanced prostate tumors. Fenofibrate (FF) has recently been pinpointed as a potential metronomic agent that augments the sensitivity of cancer cells to chemotherapeutic drugs. Here, we hypothesized that FF interferes with the drug-resistance of prostate cancer cell populations through the interference with the functions of cancer stem cell-like (SCL) cells.


Naïve and drug-resistant DU145 cells cultivated in control conditions and in the presence of DCX and/or FF were immunostained against pluripotency markers and analyzed with fluorescent microscopy, fluorescent activated cell sorting (FACS) and image stream.


FACS analyses of naïve and docetaxel (DCX)-resistant DU145 cells revealed minute sub-populations of CD133+/CD44-, CD133+/CD44+ and CD133-/CD44+ SCL cells. SCL fractions were elevated within DCX-treated naïve and DCX-resistant DU145 cell line populations. More prominent increase of SCL-fraction was also observed in naïve, and to lower extent, in drug-resistant DU145 lineages upon combined DCX/FF treatment, which confirms their drug-resistance. CD44+ cells formed the aggregates of round and loosely attached cells, surrounded by morphologically diverse cellular clusters. These SCL cells offspring displayed neoplastic and invasive phenotype similar to that of parental cells; however, they showed increased, P-gp-dependent DCX- but not DCX/FF resistance. Loss of drug-resistance over time of SCL cells offspring was accompanied by induction of their EMT and invasive potential, and combined DCX/FF treatment interfered with this process.


These observations confirm the phenotypic plasticity of SCL cells and its role in the maintenance of prostate cancer cell heterogeneity and drug-resistance. FF can enhance the efficiency of palliative prostate cancer therapies through the interference with the function of cancer stem cells.

Clinical trial identification

Editorial acknowledgement

Legal entity responsible for the study

Jagiellonian University, Faculty of Biochemistry, Biophysics and Biotechnology.


National Science Centre Poland.


All authors have declared no conflicts of interest.

This site uses cookies. Some of these cookies are essential, while others help us improve your experience by providing insights into how the site is being used.

For more detailed information on the cookies we use, please check our Privacy Policy.

Customise settings
  • Necessary cookies enable core functionality. The website cannot function properly without these cookies, and you can only disable them by changing your browser preferences.