Fenofibrate attenuates contact-stimulated cell motility and gap junctional coupling in DU-145 human prostate cancer cell populations
| Autor: | Marcin Majka, Katarzyna Miekus, Jarosław Czyż, Piotr Bonarek, Ewa Wybieralska, Krzysztof Reiss, Katarzyna Szpak, Andrzej Górecki, Justyna Drukala, Zbigniew Madeja |
|---|---|
| Rok vydání: | 2011 |
| Předmět: |
Male
connexin Cancer Research medicine.medical_specialty Cell Survival Cell Connexin Motility Cell Communication Biology Cell junction Cell membrane Fenofibrate Cell Movement Cell Line Tumor Internal medicine medicine cancer Humans Neoplasm Invasiveness PPAR alpha Viability assay reactive oxygen species Gap Junctions Prostatic Neoplasms fenofibrate General Medicine Cell cycle invasion Cell biology medicine.anatomical_structure Endocrinology motility Oncology Connexin 43 Cancer cell |
| Zdroj: | Oncology Reports. |
| ISSN: | 1791-2431 1021-335X |
| DOI: | 10.3892/or.2011.1321 |
| Popis: | In the present study, we investigated the effects of fenofibrate on the invasive potential of DU-145 human prostate cancer cells in the context of gap junctional intercellular coupling and the formation of reactive oxygen species. Time- lapse analyses of cell motility, accompanied by tests of cell viability, membrane microviscosity, reactive oxygen species accumulation and the function of gap junctional protein connexin 43 were performed in monolayer cultures of DU-145 cells following fenofibrate administration. Fenofibrate inhibited the motility of DU-145 cells and attenuated gap junctional intercellular coupling in a manner independent of its effects on cell viability, PPARα activation and cell membrane micro- viscosity. Instead, N-acetyl-L-cysteine, a scavenger of reactive oxygen species, restored cell motility and gap junctional coupling in fenofibrate-treated DU-145 cell populations. These data indicate that two parameters crucial for cancer cell metastatic potential, i.e. cell motility and gap junctional coupling, are inhibited by fenofibrate. Thus, fenofibrate affects prostate cancer cell invasion via an orchestrated action on versatile cancer cell properties determining this process. A novel mechanism of anti-invasive activity of fenofibrate, which depends on its interference with cell motility and the function of gap junctions regulated by reactive oxygen species, is suggested. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|