Molecular Mechanisms of Essential Fatty Acids and Metabolites in Regulation of Prostate Cancer Cells

2004 ◽  
Author(s):  
Charles Y. Young
Keyword(s):  
Prostate Cancer ◽  
Fatty Acids ◽  
Cancer Cells ◽  
Molecular Mechanisms ◽  
Essential Fatty Acids ◽  
Prostate Cancer Cells

scholarly journals Tumor- and osteoclast-derived NRP2 in prostate cancer bone metastases

Bone Research ◽  
2021 ◽  
Vol 9 (1) ◽  
Author(s):  
Navatha Shree Polavaram ◽  
Samikshan Dutta ◽  
Ridwan Islam ◽  
Arup K. Bag ◽  
Sohini Roy ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Bone Metastasis ◽  
Cancer Cells ◽  
Molecular Mechanisms ◽  
Osteoclast Differentiation ◽  
Potential Effect ◽  
Tumor Burden ◽  
Bone Lesions ◽  
Prostate Cancer Cells

AbstractUnderstanding the role of neuropilin 2 (NRP2) in prostate cancer cells as well as in the bone microenvironment is pivotal in the development of an effective targeted therapy for the treatment of prostate cancer bone metastasis. We observed a significant upregulation of NRP2 in prostate cancer cells metastasized to bone. Here, we report that targeting NRP2 in cancer cells can enhance taxane-based chemotherapy with a better therapeutic outcome in bone metastasis, implicating NRP2 as a promising therapeutic target. Since, osteoclasts present in the tumor microenvironment express NRP2, we have investigated the potential effect of targeting NRP2 in osteoclasts. Our results revealed NRP2 negatively regulates osteoclast differentiation and function in the presence of prostate cancer cells that promotes mixed bone lesions. Our study further delineated the molecular mechanisms by which NRP2 regulates osteoclast function. Interestingly, depletion of NRP2 in osteoclasts in vivo showed a decrease in the overall prostate tumor burden in the bone. These results therefore indicate that targeting NRP2 in prostate cancer cells as well as in the osteoclastic compartment can be beneficial in the treatment of prostate cancer bone metastasis.

Newly synthesized benzimidazoles inhibits vascular endothelial growth factor and matrix metalloproteinase-2 and -9 levels in prostate cancer cells

2021 ◽  
Vol 21 ◽  
Author(s):  
Suleyman Ilhan ◽  
Gamze Dilekci ◽  
Adem Guner ◽  
Hakan Bektas
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Molecular Mechanisms ◽  
Umbilical Vein ◽  
Imidazole Ring ◽  
Matrix Metalloproteinase 2 ◽  
Benzimidazole Derivatives ◽  
Prostate Cancer Cells ◽  
Protein Levels ◽  
Umbilical Vein Endothelial Cells

Background: Investigating the effects of newly synthesized agents on various molecular mechanisms to understand their mechanism of action is an important step of pre-clinical screening. Benzimidazoles are composed of a unique fused benzene and imidazole ring and have attracted great attention due to their broad bioactivities, including antitumor. Objective: In the current study, we reported the synthesis of novel benzimidazole derivatives and investigated the possible cytotoxic and anti-angiogenic effects on human prostate cancer and umbilical vein endothelial cells (HUVECs). Methods: MTT assay was used to assess cell viability. A scratch assay was conducted to monitor the migration of cells. mRNA expression levels of VEGF, MMP-2, and MMP-9 were evaluated using qPCR. Changes in protein levels were evaluated by western blotting. Results: Compound G1, having a chlorine moiety, showed a potent cytotoxic activity on both prostate cancer cells and HUVECs, and inhibited cell migration via decreasing the mRNA and protein levels of key angiogenesis-related molecules such as VEGF, MMP-2, and MMP-9. Conclusion: These results suggest that newly synthesized G1 may be a novel anti-angiogenic agent for prostate cancer treatment.

Molecular mechanisms of plant steroids and study of their interaction with nuclear receptors in prostate cancer cells

2020 ◽  
Vol 137 ◽  
pp. 111164 ◽  
Author(s):  
Zlata Huskova ◽  
Jana Steigerova ◽  
Jana Oklestkova ◽  
Lucie Rarova ◽  
Zdenek Kolar ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Nuclear Receptors ◽  
Molecular Mechanisms ◽  
Prostate Cancer Cells

scholarly journals Omega-3 Fatty Acids and Other FFA4 Agonists Inhibit Growth Factor Signaling in Human Prostate Cancer Cells

2014 ◽  
Vol 352 (2) ◽  
pp. 380-394 ◽  
Author(s):  
Ze Liu ◽  
Mandi M. Hopkins ◽  
Zhihong Zhang ◽  
Chrystal B. Quisenberry ◽  
Louise C. Fix ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Fatty Acids ◽  
Growth Factor ◽  
Cancer Cells ◽  
Human Prostate ◽  
Growth Factor Signaling ◽  
Human Prostate Cancer ◽  
Omega 3 Fatty Acids ◽  
Omega 3 ◽  
Prostate Cancer Cells

scholarly journals Regulation of cell–cell adhesion in prostate cancer cells by microRNA-96 through upregulation of E-Cadherin and EpCAM

2019 ◽  
Vol 41 (7) ◽  
pp. 865-874
Author(s):  
Gjendine Voss ◽  
Benedikta S Haflidadóttir ◽  
Helena Järemo ◽  
Margareta Persson ◽  
Tina Catela Ivkovic ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Adhesion ◽  
Bone Metastasis ◽  
Cancer Cells ◽  
Molecular Mechanisms ◽  
Cell Interaction ◽  
Metastatic Progression ◽  
Prostate Cancer Cells ◽  
E Cadherin ◽  
Cell Cell

Abstract Prostate cancer is one of the most common cancers in men, yet the biology behind lethal disease progression and bone metastasis is poorly understood. In this study, we found elevated levels of microRNA-96 (miR-96) in prostate cancer bone metastasis samples. To determine the molecular mechanisms by which miR-96 deregulation contributes to metastatic progression, we performed an Argonaute2-immunoprecipitation assay, in which mRNAs associated with cell–cell interaction were enriched. The expression of two cell adhesion molecules, E-Cadherin and EpCAM, was upregulated by miR-96, and potential targets sites were identified in the coding sequences of their mRNAs. We further showed that miR-96 enhanced cell–cell adhesion between prostate cancer cells as well as their ability to bind to osteoblasts. Our findings suggest that increased levels of miR-96 give prostate cancer cells an advantage at forming metastases in the bone microenvironment due to increased cell–cell interaction. We propose that miR-96 promotes bone metastasis in prostate cancer patients by facilitating the outgrowth of macroscopic tumours in the bone.

scholarly journals Nuclear localization of parathyroid hormone-related peptide confers resistance to anoikis in prostate cancer cells

2012 ◽  
Vol 19 (3) ◽  
pp. 243-254 ◽  
Author(s):  
Serk In Park ◽  
Laurie K McCauley
Keyword(s):  
Gene Expression ◽  
Prostate Cancer ◽  
Parathyroid Hormone ◽  
Cancer Cells ◽  
Nuclear Localization ◽  
Molecular Mechanisms ◽  
Lncap Cells ◽  
Prostate Cancer Cells ◽  
Related Peptide ◽  
Parathyroid Hormone Related Peptide

Prostate cancer remains a leading cause of cancer-related death in men, largely attributable to distant metastases, most frequently to bones. Despite intensive investigations, molecular mechanisms underlying metastasis are not completely understood. Among prostate cancer-derived factors, parathyroid hormone-related peptide (PTHrP), first discovered as an etiologic factor for malignancy-induced hypercalcemia, regulates many cellular functions critical to tumor growth, angiogenesis, and metastasis. In this study, the role of PTHrP in tumor cell survival from detachment-induced apoptosis (i.e. anoikis) was investigated. Reduction ofPTHLH(encoding PTHrP) gene expression in human prostate cancer cells (PC-3) increased the percentage of apoptotic cells when cultured in suspension. Conversely, overexpression of PTHrP protected prostate cancer cells (Ace-1 and LNCaP, both typically expressing low or undetectable basal PTHrP) from anoikis. Overexpression of nuclear localization signal (NLS)-defective PTHrP failed to protect cells from anoikis, suggesting that PTHrP-dependent protection from anoikis is an intracrine event. A PCR-based apoptosis-related gene array showed that detachment increased expression of theTNFgene (encoding the proapoptotic protein tumor necrosis factor-α) fourfold greater in PTHrP-knockdown PC-3 cells than in control PC-3 cells. In parallel,TNFgene expression was significantly reduced in PTHrP-overexpressing LNCaP cells, but not in NLS-defective PTHrP overexpressing LNCaP cells, when compared with control LNCaP cells. Subsequently, in a prostate cancer skeletal metastasis mouse model, PTHrP-knockdown PC-3 cells resulted in significantly fewer metastatic lesions compared to control PC-3 cells, suggesting that PTHrP mediated antianoikis events in the bloodstream. In conclusion, nuclear localization of PTHrP confers prostate cancer cell resistance to anoikis, potentially contributing to prostate cancer metastasis.

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