The Impact of Centrosome Pathologies on Prostate Cancer Development and Progression

2018 ◽  
pp. 67-81 ◽  
Author(s):  
Heide Schatten ◽  
Maureen O. Ripple
Keyword(s):  
Prostate Cancer ◽  
Cancer Development ◽  
Prostate Cancer Development ◽  
The Impact

scholarly journals Both p110α and p110β isoforms of PI3K can modulate the impact of loss-of-function of the PTEN tumour suppressor

2012 ◽  
Vol 442 (1) ◽  
pp. 151-159 ◽  
Author(s):  
Inma M. Berenjeno ◽  
Julie Guillermet-Guibert ◽  
Wayne Pearce ◽  
Alexander Gray ◽  
Stewart Fleming ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Lines ◽  
Tumour Suppressor ◽  
Negative Regulator ◽  
Cancer Development ◽  
Pten Loss ◽  
Mouse Tissues ◽  
Primary Mouse ◽  
Prostate Cancer Development ◽  
The Impact

The PI3K (phosphoinositide 3-kinase) pathway is commonly activated in cancer as a consequence of inactivation of the tumour suppressor PTEN (phosphatase and tensin homologue deleted on chromosome 10), a major negative regulator of PI3K signalling. In line with this important role of PTEN, mice that are heterozygous for a PTEN-null allele (PTEN+/− mice) spontaneously develop a variety of tumours in multiple organs. PTEN is a phosphatase with selectivity for PtdIns(3,4,5)P3, which is produced by the class I isoforms of PI3K (p110α, p110β, p110γ and p110δ). Previous studies indicated that PTEN-deficient cancer cell lines mainly depend on p110β, and that p110β, but not p110α, controls mouse prostate cancer development driven by PTEN loss. In the present study, we investigated whether the ubiquitously expressed p110α can also functionally interact with PTEN in cancer. Using genetic mouse models that mimic systemic administration of p110α- or p110β-selective inhibitors, we confirm that inactivation of p110β, but not p110α, inhibits prostate cancer development in PTEN+/− mice, but also find that p110α inactivation protects from glomerulonephritis, pheochromocytoma and thyroid cancer induced by PTEN loss. This indicates that p110α can modulate the impact of PTEN loss in disease and tumourigenesis. In primary and immortalized mouse fibroblast cell lines, both p110α and p110β controlled steady-state PtdIns(3,4,5)P3 levels and Akt signalling induced by heterozygous PTEN loss. In contrast, no correlation was found in primary mouse tissues between PtdIns(3,4,5)P3 levels, PI3K/PTEN genotype and cancer development. Taken together, our results from the present study show that inactivation of either p110α or p110β can counteract the impact of PTEN inactivation. The potential implications of these findings for PI3K-targeted therapy of cancer are discussed.

The impact of hypertriglyceridemia on prostate cancer development in patients aged ≥60 years

2011 ◽  
Vol 109 (4) ◽  
pp. 515-519 ◽  
Author(s):  
Norihiro Hayashi ◽  
Masato Matsushima ◽  
Toshihiro Yamamoto ◽  
Hiroshi Sasaki ◽  
Hiroyuki Takahashi ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Development ◽  
Prostate Cancer Development ◽  
The Impact

scholarly journals The Impact of Diabetes on the Risk of Prostate Cancer Development according to Body Mass Index: A 10-year Nationwide Cohort Study

2016 ◽  
Vol 7 (14) ◽  
pp. 2061-2066 ◽  
Author(s):  
Jin Bong Choi ◽  
Hyong Woo Moon ◽  
Young Hyun Park ◽  
Woong Jin Bae ◽  
Hyuk Jin Cho ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Body Mass Index ◽  
Cohort Study ◽  
Body Mass ◽  
Cancer Development ◽  
Prostate Cancer Development ◽  
The Impact

scholarly journals Research Evidence on High-Fat Diet-Induced Prostate Cancer Development and Progression

2019 ◽  
Vol 8 (5) ◽  
pp. 597 ◽  
Author(s):  
Shintaro Narita ◽  
Taketoshi Nara ◽  
Hiromi Sato ◽  
Atsushi Koizumi ◽  
Mingguo Huang ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Dietary Fat ◽  
High Fat Diet ◽  
Cancer Development ◽  
Preclinical Studies ◽  
Preclinical Models ◽  
High Fat ◽  
Prostate Cancer Development ◽  
Underlying Mechanisms ◽  
The Impact

Although recent evidence has suggested that a high-fat diet (HFD) plays an important role in prostate carcinogenesis, the underlying mechanisms have largely remained unknown. This review thus summarizes previous preclinical studies that have used prostate cancer cells and animal models to assess the impact of dietary fat on prostate cancer development and progression. Large variations in the previous studies were found during the selection of preclinical models and types of dietary intervention. Subcutaneous human prostate cancer cell xenografts, such as LNCaP, LAPC-4, and PC-3 and genetic engineered mouse models, such as TRAMP and Pten knockout, were frequently used. The dietary interventions had not been standardized, and distinct variations in the phenotype were observed in different studies using distinct HFD components. The use of different dietary components in the research models is reported to influence the effect of diet-induced metabolic disorders. The proposed underlying mechanisms for HFD-induced prostate cancer were divided into (1) growth factor signaling, (2) lipid metabolism, (3) inflammation, (4) hormonal modulation, and others. A number of preclinical studies proposed that dietary fat and/or obesity enhanced prostate cancer development and progression. However, the relationship still remains controversial, and care should be taken when interpreting the results in a human context. Future studies using more sophisticated preclinical models are imperative in order to explore deeper understanding regarding the impact of dietary fat on the development and progression of prostate cancer.

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