Cellular mechanisms of taxane therapy in castration resistant prostate cancer
(2014) In Lund University Faculty of Medicine Doctoral Dissertation Series 119.- Abstract
- Chemotherapy of castration resistant prostate cancer (CRPC) is based on taxane formulations worldwide. Only 30-50 % of patients respond to this therapy and the exact cellular mechanisms of taxane resistance in PC cells are not fully elucidated. There is convincing evidence that androgen receptor (AR) is affected by exposure to these compounds. The studies presented in this doctoral thesis identify c-jun, a proto-oncogene as a crucial key player which interacts with AR and thus determines the outcome of taxane therapy. We show that AR and c-jun physically interact on protein and gene level and this interaction is taxane specific. This results in different expression levels of AR regulated genes evidenced in alterations of PSA, KLK2 and... (More)
- Chemotherapy of castration resistant prostate cancer (CRPC) is based on taxane formulations worldwide. Only 30-50 % of patients respond to this therapy and the exact cellular mechanisms of taxane resistance in PC cells are not fully elucidated. There is convincing evidence that androgen receptor (AR) is affected by exposure to these compounds. The studies presented in this doctoral thesis identify c-jun, a proto-oncogene as a crucial key player which interacts with AR and thus determines the outcome of taxane therapy. We show that AR and c-jun physically interact on protein and gene level and this interaction is taxane specific. This results in different expression levels of AR regulated genes evidenced in alterations of PSA, KLK2 and NKX3.1 in a castration resistant cell model. Sustained downregulation of c-jun results in a significant increased efficacy of taxane therapy confirming that c-jun acts as a potent antiapoptotic factor. A major drawback of taxane compound is also their ability to reach the tumor cells in sufficient concentration. Studies performed in a xenograft model showed that a novel liquid crystal nanoparticle formulation of docetaxel (LNCP/docetaxel) more efficiently decreased tumor size with less side effects than the commercially available docetaxel. Taken together, our stydies identify c-jun as a key regulator of taxnae therapy. Targeting c-jun in combination with taxane treatment may increase efficacy of chemotherapy in future. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/4698349
- author
- Tinzl, Martina LU
- supervisor
- opponent
-
- Prof Guido, Jenster, Erasmus MC, Rotterdam
- organization
- publishing date
- 2014
- type
- Thesis
- publication status
- published
- subject
- keywords
- Prostate cancer, chemotherapy, taxane, c-jun, androgen receptor, PSA
- in
- Lund University Faculty of Medicine Doctoral Dissertation Series
- volume
- 119
- pages
- 120 pages
- publisher
- Division of urological research
- defense location
- CRC Aula, Jan Waldenströmsgata 35, Skånes Universitetssjukhus i Malmö.
- defense date
- 2014-11-08 09:00:00
- ISSN
- 1652-8220
- ISBN
- 978-91-7619-048-7
- language
- English
- LU publication?
- yes
- id
- ca233025-848f-4c76-96a8-11b228a0cc6d (old id 4698349)
- date added to LUP
- 2016-04-01 14:33:40
- date last changed
- 2023-04-18 20:12:10
@phdthesis{ca233025-848f-4c76-96a8-11b228a0cc6d, abstract = {{Chemotherapy of castration resistant prostate cancer (CRPC) is based on taxane formulations worldwide. Only 30-50 % of patients respond to this therapy and the exact cellular mechanisms of taxane resistance in PC cells are not fully elucidated. There is convincing evidence that androgen receptor (AR) is affected by exposure to these compounds. The studies presented in this doctoral thesis identify c-jun, a proto-oncogene as a crucial key player which interacts with AR and thus determines the outcome of taxane therapy. We show that AR and c-jun physically interact on protein and gene level and this interaction is taxane specific. This results in different expression levels of AR regulated genes evidenced in alterations of PSA, KLK2 and NKX3.1 in a castration resistant cell model. Sustained downregulation of c-jun results in a significant increased efficacy of taxane therapy confirming that c-jun acts as a potent antiapoptotic factor. A major drawback of taxane compound is also their ability to reach the tumor cells in sufficient concentration. Studies performed in a xenograft model showed that a novel liquid crystal nanoparticle formulation of docetaxel (LNCP/docetaxel) more efficiently decreased tumor size with less side effects than the commercially available docetaxel. Taken together, our stydies identify c-jun as a key regulator of taxnae therapy. Targeting c-jun in combination with taxane treatment may increase efficacy of chemotherapy in future.}}, author = {{Tinzl, Martina}}, isbn = {{978-91-7619-048-7}}, issn = {{1652-8220}}, keywords = {{Prostate cancer; chemotherapy; taxane; c-jun; androgen receptor; PSA}}, language = {{eng}}, publisher = {{Division of urological research}}, school = {{Lund University}}, series = {{Lund University Faculty of Medicine Doctoral Dissertation Series}}, title = {{Cellular mechanisms of taxane therapy in castration resistant prostate cancer}}, volume = {{119}}, year = {{2014}}, }