scholarly journals The Novel PIM1 Inhibitor NMS-P645 Reverses PIM1-Dependent Effects on TMPRSS2/ERG Positive Prostate Cancer Cells And Shows Anti-Proliferative Activity in Combination with PI3K Inhibition

2017 ◽  
Vol 8 (1) ◽  
pp. 140-145 ◽  
Author(s):  
Luca Mologni ◽  
Vera Magistroni ◽  
Francesco Casuscelli ◽  
Marisa Montemartini ◽  
Carlo Gambacorti-Passerini
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Proliferative Activity ◽  
The Novel ◽  
Prostate Cancer Cells ◽  
Pi3k Inhibition

scholarly journals The cytotoxic and pro-apoptotic activities of the novel fluoropyrimidine F10 towards prostate cancer cells are enhanced by Zn2+ -chelation and inhibiting the serine protease Omi/HtrA2

The Prostate ◽  
2014 ◽  
Vol 75 (4) ◽  
pp. 360-369 ◽  
Author(s):  
William H. Gmeiner ◽  
Olcay Boyacioglu ◽  
Christopher H. Stuart ◽  
Jamie Jennings-Gee ◽  
K.C. Balaji
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Serine Protease ◽  
The Novel ◽  
Prostate Cancer Cells

scholarly journals miRNA-205 Nanoformulation Sensitizes Prostate Cancer Cells to Chemotherapy

Cancers ◽  
2018 ◽  
Vol 10 (9) ◽  
pp. 289 ◽  
Author(s):  
Prashanth Nagesh ◽  
Pallabita Chowdhury ◽  
Elham Hatami ◽  
Vijaya Boya ◽  
Vivek Kashyap ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Confocal Imaging ◽  
The Novel ◽  
Prostate Cancer Cells ◽  
Study Results ◽  
Docetaxel Treatment ◽  
Iron Oxide Core ◽  
Poly Ethylene ◽  
Microrna Delivery

The therapeutic application of microRNA(s) in the field of cancer has generated significant attention in research. Previous studies have shown that miR-205 negatively regulates prostate cancer cell proliferation, metastasis, and drug resistance. However, the delivery of miR-205 is an unmet clinical need. Thus, the development of a viable nanoparticle platform to deliver miR-205 is highly sought. A novel magnetic nanoparticle (MNP)-based nanoplatform composed of an iron oxide core with poly(ethyleneimine)-poly(ethylene glycol) layer(s) was developed. An optimized nanoplatform composition was confirmed by examining the binding profiles of MNPs with miR-205 using agarose gel and fluorescence methods. The novel formulation was applied to prostate cancer cells for evaluating cellular uptake, miR-205 delivery, and anticancer, antimetastasis, and chemosensitization potentials against docetaxel treatment. The improved uptake and efficacy of formulations were studied with confocal imaging, flow cytometry, proliferation, clonogenicity, Western blot, q-RT-PCR, and chemosensitization assays. Our findings demonstrated that the miR-205 nanoplatform induces significant apoptosis and enhancing chemotherapeutic effects in prostate cancer cells. Overall, these study results provide a strong proof-of-concept for a novel nonviral-based nanoparticle protocol for effective microRNA delivery to prostate cancer cells.

scholarly journals MP51-09 THE NOVEL ROLE OF SPOP IN REGULATING TOPOISOMERASE 2A IN PROSTATE CANCER CELLS AS A POTENTIAL THERAPEUTIC MARKER FOR DNA REPAIR TARGETED THERAPY

2020 ◽  
Vol 203 ◽  
pp. e767
Author(s):  
Ryuta Watanabe* ◽  
Masashi Maekawa ◽  
Miki Hieda ◽  
Tomohiko Taguchi ◽  
Noriyoshi Miura ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Dna Repair ◽  
Targeted Therapy ◽  
Cancer Cells ◽  
The Novel ◽  
Prostate Cancer Cells ◽  
Topoisomerase 2A

Amiloride effects on abiraterone antiproliferative activity in prostate cancer cells in vitro and on clinical management of abiraterone induced mineralocorticoid excess syndrome.

2016 ◽  
Vol 34 (2_suppl) ◽  
pp. 175-175 ◽  
Author(s):  
Francesca Valcamonico ◽  
Francesca Bedussi ◽  
Diego Galli ◽  
Alberto Dalla Volta ◽  
Martina Fragni ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Clinical Management ◽  
Proliferative Activity ◽  
Complete Disappearance ◽  
Dependent Manner ◽  
Prostate Cancer Cells ◽  
Androgen Synthesis ◽  
Aldosterone Receptor

175 Background: Abiraterone acetate (AA) deeply inhibits androgen synthesis but leads to an ACTH driven increase in mineralocorticoid hormones requiring glucocorticoid supplementation that may impair its antineoplastic efficacy. New strategies for the management of the AA induced mineral corticoid excess syndrome (MCES) are warranted. Methods: We analyzed in vitro the interaction in terms of proliferative activity of AA plus/minus prednisone with the steroid aldosterone receptor antagonists: eplerenone, spironolactone, a non-steroidal aldosterone receptor antagonist (PF-03882845) and the epithelial sodium channel antagonist amiloride. LNCaP were grown in a medium with charcoal-treated serum and concentration-response curves for each studied drug were performed. Besides, the activity of amiloride plus hydrochlorothiazide was assessed in the clinical management of AA induced MCES in 5 consecutive patients with castrate resistant prostate cancer. The recovery of AA induced MCES symptoms and signs was the primary end point. Results: Prednisone, spironolactone and eplerenone induced an increase in the LNCAP proliferation rate and antagonized the AA-induced reduction of the cell proliferation in a concentration-dependent manner, while PF-03882845 did not. Amiloride at high concentrations induced cell death. When combined with AA +/- prednisone, amiloride at low concentration did not interfere with AA anti-proliferative activity however an additive inhibitory effect was observed at higher concentrations. The association of amiloride with hydrochlorothiazide led to a complete disappearance of all clinical and biochemical signs of abiraterone induced MCES in the 5 treated patients. Conclusions: Amiloride and PF-03882845 do not negatively interfere with the AA inhibition of proliferative activity of prostate cancer cells in vitro. The association of amiloride plus hydrochlorothiazide is efficacious in the management AA induced MCES.

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