Advanced prostate cancer &amp;ndash; patient survival and potential impact of enzalutamide and other emerging therapies

Patel, Nisarg; Finianos, Antoine; Whitaker, Katrine B.; Aragon‐Ching, Jeanny B.

doi:10.2147/tcrm.s57509

Cited by 6 publications

(5 citation statements)

References 91 publications

(108 reference statements)

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“…Recurrence and side effects of chemotherapy drugs are the bottleneck of prostate cancer therapy 2 , 3 , 9 . Anti-cancer drugs with reduced side effect are thus required for long-term therapy and prevention of prostate cancer 32 .…”

Section: Discussionmentioning

confidence: 99%

“…Inhibition of prostate cancer CSCs, therefore, has emerged as a new therapeutic strategy 7 , 8 . On the other hand, chemotherapy drugs and other novel drugs used for prostate cancer, such as enzalutamide and abiraterone, are aggressive and all have adverse side effects 9 ; Thus, natural compounds, which inhibit CSCs may prove to be promising agents for prostate cancer therapy 10 .…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Luteolin attenuates Wnt signaling via upregulation of FZD6 to suppress prostate cancer stemness revealed by comparative proteomics

Han¹,

Lang

Zhang³

et al. 2018

Sci Rep

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The mechanisms underlying luteolin-induced inhibition of prostate cancer (PCa) stemness have remained elusive. Here, we report that luteolin suppresses PCa stemness through Wnt signaling by upregulation of FZD6 (frizzled class receptor 6). Luteolin inhibits PCa cell proliferation, migration, self-renewal as well as the expression of prostate cancer stem cell markers in vitro. Through iTRAQ-based quantitative proteomics study, we identified 208 differentially expressed proteins in luteolin-treated PC-3 cells. Subsequent mechanistic analysis revealed that luteolin inhibits Wnt signaling by transcriptional upregulation of FZD6, and thereby suppressing the stemness of PCa cells. Furthermore, we identified FZD6 as a tumor suppressor that can abolish PCa stemness. In summary, our findings demonstrate that suppression of Wnt signaling by upregulation of FZD6 is a mechanism underlying luteolin-induced inhibition of PCa stemness. Our work suggests a new therapeutic strategy against human prostate cancer caused by aberrant activation of Wnt signaling.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Luteolin attenuates Wnt signaling via upregulation of FZD6 to suppress prostate cancer stemness revealed by comparative proteomics

Han¹,

Lang

Zhang³

et al. 2018

Sci Rep

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“…There may be a good chance that the observed stagnation in the PPS may be overcome in the near future when newly developed and approved agents keep their promises in metastatic castrate-resistant prostate cancer [23]. …”

Section: Discussionmentioning

confidence: 99%

Changes in Prognostic and Therapeutic Parameters in Prostate Cancer from an Epidemiological View over 20 Years

et al. 2015

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Background: The study objective was to examine changes in prognosis and treatment of prostate cancer patients over 20 years and to evaluate their impact on survival. Patients and Methods: 38,861 prostate cancer patients diagnosed between 1990 and 2010 and living in the catchment area of the Munich Cancer Registry were analysed. Results: Pre-therapeutic prostate-specific antigen (PSA) testing increased substantially in the early 1990s. A shift from capsule-exceeding tumours to capsule-limited tumours also took place especially in the 1990s. The proportion of radical prostatectomy increased continuously over the last 20 years from 20% to almost 50% whereas hormone therapy decreased from 55% to 18%. Radiation therapy and transurethral resection of the prostate increased slightly from about 5% to 10%. The 5- and 10-year relative survival rates increased from 92% to 97% and from 86% to 92%, respectively. Conclusions: 2 reasons may account for the rise in survival rates over 20 years: First, the establishment of widely used PSA testing resulted in a shift towards more favourable T categories due to the detection of many additional small tumours as well as the noticeable change in initial treatment strategy towards more radical prostatectomies. The second factor that likely increased survival was improvements in the therapies themselves.

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“…One of the main challenges in prostate cancer is effective treatment of castration resistant disease. Although the FDA recently approved several new therapies including Enzalutamide, Abiraterone, Provenge and Xofigo, the survival advantage is limited to a few months (1). Thus, better options to more effectively treat advanced prostate cancer are needed.…”

Section: Introductionmentioning

confidence: 99%

The Sphingosine Kinase 2 Inhibitor ABC294640 Reduces the Growth of Prostate Cancer Cells and Results in Accumulation of Dihydroceramides In Vitro and In Vivo

Venant

Rahmaniyan

Jones

et al. 2015

Molecular Cancer Therapeutics

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Despite recent advances in the development of novel therapies against castration resistant prostate cancer, the advanced form of the disease remains a major treatment challenge. Aberrant sphingolipid signaling through sphingosine kinases and their product sphingosine-1-phosphate can promote proliferation, drug resistance, angiogenesis and inflammation. The sphingosine kinase 2 inhibitor ABC294640 is undergoing clinical testing in cancer patients, and in this study we investigated the effects this first-in-class inhibitor in castration resistant prostate cancer. In vitro, ABC294640 decreased prostate cancer cell viability as well as the expression of c-Myc and the androgen receptor while lysosomal acidification increased. ABC294640 also induced a greater than 3-fold increase in dihydroceramides that inversely correlated with inhibition of dihydroceramide desaturase (DEGS) activity. Expression of sphingosine kinase 2 was dispensable for the ABC294640-mediated increase in dihydroceramides. In vivo, ABC294640 diminished the growth rate of TRAMP-C2 xenografts in syngeneic hosts and elevated dihydroceramides within tumors as visualized by MALDI imaging mass spectroscopy. The plasma of ABC294640 treated mice contained significantly higher levels of C16- and C24:1-ceramides (but not dihydro-C16-ceramide) compared to vehicle treated mice. In summary, our results suggest that ABC294640 may reduce the proliferative capacity of castration resistant prostate cancer cells through both, inhibition of sphingosine kinase 2 and dihydroceramide desaturase, which provides a foundation for future exploration of this small molecule inhibitor for the treatment of advanced disease.

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Advanced prostate cancer – patient survival and potential impact of enzalutamide and other emerging therapies

Cited by 6 publications

References 91 publications

Luteolin attenuates Wnt signaling via upregulation of FZD6 to suppress prostate cancer stemness revealed by comparative proteomics

Luteolin attenuates Wnt signaling via upregulation of FZD6 to suppress prostate cancer stemness revealed by comparative proteomics

Changes in Prognostic and Therapeutic Parameters in Prostate Cancer from an Epidemiological View over 20 Years

The Sphingosine Kinase 2 Inhibitor ABC294640 Reduces the Growth of Prostate Cancer Cells and Results in Accumulation of Dihydroceramides In Vitro and In Vivo

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