scholarly journals A Novel Cutaneous Fatty Acid-Binding Protein-Related Signaling Pathway Leading to Malignant Progression in Prostate Cancer Cells

2013 ◽  
Vol 4 (7-8) ◽  
pp. 297-314 ◽  
Author(s):  
Z. Bao ◽  
M. I. Malki ◽  
S. S. Forootan ◽  
J. Adamson ◽  
F. S. Forootan ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Fatty Acid ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Fatty Acid Binding Protein ◽  
Binding Protein ◽  
Malignant Progression ◽  
Prostate Cancer Cells ◽  
Fatty Acid Binding ◽  
Acid Binding Protein

scholarly journals Involvement of Fatty Acid Binding Protein 5 and PPARβ/δin Prostate Cancer Cell Growth

PPAR Research ◽  
2010 ◽  
Vol 2010 ◽  
pp. 1-9 ◽  
Author(s):  
Elwin Morgan ◽  
Padmamalini Kannan-Thulasiraman ◽  
Noa Noy
Keyword(s):  
Prostate Cancer ◽  
Fatty Acid ◽  
Cancer Cell ◽  
Fatty Acid Binding Protein ◽  
Target Genes ◽  
Prostate Cancer Cell ◽  
Binding Protein ◽  
Fatty Acid Binding ◽  
General Role ◽  
Acid Binding Protein

Fatty acid binding protein 5 (FABP5) delivers ligands from the cytosol directly to the nuclear receptor PPARβ/δand thus facilitates the ligation and enhances the transcriptional activity of the receptor. We show here that expression levels of both FABP5 and PPARβ/δare correlated with the tumorigenic potential of prostate cancer cell lines. We show further that FABP5 comprises a direct target gene for PPARβ/δand thus the binding protein and its cognate receptor are engaged in a positive feedback loop. The observations demonstrate that, similarly to effects observed in mammary carcinomas, activation of the FABP5/PPARβ/δpathway induces PPARβ/δtarget genes involved in cell survival and growth and enhances cell proliferation and anchorage-independent growth in prostate cancer cells. Furthermore, the data show that downregulation of either FABP5 or PPARβ/δinhibits the growth of the highly malignant prostate cancer PC3M cells. These studies suggest that the FABP5/PPARβ/δpathway may play a general role in facilitating tumor progression and that inhibition of the pathway may comprise a novel strategy in treatment of cancer.

scholarly journals Docetaxel/cabazitaxel and fatty acid binding protein 5 inhibitors produce synergistic inhibition of prostate cancer growth

The Prostate ◽  
2019 ◽  
Vol 80 (1) ◽  
pp. 88-98 ◽  
Author(s):  
Gregory Carbonetti ◽  
Cynthia Converso ◽  
Timothy Clement ◽  
Changwei Wang ◽  
Lloyd C Trotman ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Fatty Acid ◽  
Fatty Acid Binding Protein ◽  
Binding Protein ◽  
Cancer Growth ◽  
Fatty Acid Binding ◽  
Synergistic Inhibition ◽  
Acid Binding Protein

scholarly journals An Amplified Fatty Acid-Binding Protein Gene Cluster in Prostate Cancer: Emerging Roles in Lipid Metabolism and Metastasis

Cancers ◽  
2020 ◽  
Vol 12 (12) ◽  
pp. 3823
Author(s):  
Rong-Zong Liu ◽  
Roseline Godbout
Keyword(s):  
Prostate Cancer ◽  
Fatty Acid ◽  
Gene Cluster ◽  
Fatty Acid Binding Protein ◽  
Binding Protein ◽  
Cohort Analysis ◽  
Chromosome 8 ◽  
Molecular Pathways ◽  
Fatty Acid Binding ◽  
Acid Binding Protein

Treatment for early stage and localized prostate cancer (PCa) is highly effective. Patient survival, however, drops dramatically upon metastasis due to drug resistance and cancer recurrence. The molecular mechanisms underlying PCa metastasis are complex and remain unclear. It is therefore crucial to decipher the key genetic alterations and relevant molecular pathways driving PCa metastatic progression so that predictive biomarkers and precise therapeutic targets can be developed. Through PCa cohort analysis, we found that a fatty acid-binding protein (FABP) gene cluster (containing five FABP family members) is preferentially amplified and overexpressed in metastatic PCa. All five FABP genes reside on chromosome 8 at 8q21.13, a chromosomal region frequently amplified in PCa. There is emerging evidence that these FABPs promote metastasis through distinct biological actions and molecular pathways. In this review, we discuss how these FABPs may serve as drivers/promoters for PCa metastatic transformation using patient cohort analysis combined with a review of the literature.

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