Analysis of the R1881-regulated AR, HOXB13 and FOXA1 cistromes in LHSAR or LNCaP prostate cancer cells, or in normal or primary prostate tumor tissue

2019 ◽  
Author(s):  
MM Pomerantz
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Tumor Tissue ◽  
Prostate Tumor ◽  
Prostate Cancer Cells ◽  
Primary Prostate Tumor

scholarly journals Unbiased Phenotype-Based Screen Identifies Therapeutic Agents Selective for Metastatic Prostate Cancer

2021 ◽  
Vol 10 ◽  
Author(s):  
Ivy Chung ◽  
Kun Zhou ◽  
Courtney Barrows ◽  
Jacqueline Banyard ◽  
Arianne Wilson ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Tumor Cells ◽  
Metastatic Prostate Cancer ◽  
Prostate Tumor ◽  
Prostate Cancer Cells ◽  
Normal Prostate ◽  
Prostate Tumor Cells ◽  
Benign Prostate

In American men, prostate cancer is the second leading cause of cancer-related death. Dissemination of prostate cancer cells to distant organs significantly worsens patients’ prognosis, and currently there are no effective treatment options that can cure advanced-stage prostate cancer. In an effort to identify compounds selective for metastatic prostate cancer cells over benign prostate cancer cells or normal prostate epithelial cells, we applied a phenotype-based in vitro drug screening method utilizing multiple prostate cancer cell lines to test 1,120 different compounds from a commercial drug library. Top drug candidates were then examined in multiple mouse xenograft models including subcutaneous tumor growth, experimental lung metastasis, and experimental bone metastasis assays. A subset of compounds including fenbendazole, fluspirilene, clofazimine, niclosamide, and suloctidil showed preferential cytotoxicity and apoptosis towards metastatic prostate cancer cells in vitro and in vivo. The bioavailability of the most discerning agents, especially fenbendazole and albendazole, was improved by formulating as micelles or nanoparticles. The enhanced forms of fenbendazole and albendazole significantly prolonged survival in mice bearing metastases, and albendazole-treated mice displayed significantly longer median survival times than paclitaxel-treated mice. Importantly, these drugs effectively targeted taxane-resistant tumors and bone metastases – two common clinical conditions in patients with aggressive prostate cancer. In summary, we find that metastatic prostate tumor cells differ from benign prostate tumor cells in their sensitivity to certain drug classes. Taken together, our results strongly suggest that albendazole, an anthelmintic medication, may represent a potential adjuvant or neoadjuvant to standard therapy in the treatment of disseminated prostate cancer.

Prostate Tumor-Inducing Gene-1 Analysis in Human Prostate Cancer Cells and Tissue in Relation toMycoplasmaInfection

2008 ◽  
Vol 26 (8) ◽  
pp. 800-808 ◽  
Author(s):  
Bruna Scaggiante ◽  
Serena Bonin ◽  
Luigi Cristiano ◽  
Salvatore Siracusano ◽  
Giorgio Stanta ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Prostate Tumor ◽  
Human Prostate ◽  
Human Prostate Cancer ◽  
Prostate Cancer Cells

scholarly journals Systematic Identification of MicroRNAs That Impact on Proliferation of Prostate Cancer Cells and Display Changed Expression in Tumor Tissue

2016 ◽  
Vol 69 (6) ◽  
pp. 1120-1128 ◽  
Author(s):  
Anna Aakula ◽  
Pekka Kohonen ◽  
Suvi-Katri Leivonen ◽  
Rami Mäkelä ◽  
Petteri Hintsanen ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Tumor Tissue ◽  
Prostate Cancer Cells ◽  
Systematic Identification

scholarly journals SULT2B1b Sulfotransferase: Induction by Vitamin D Receptor and Reduced Expression in Prostate Cancer

2013 ◽  
Vol 27 (6) ◽  
pp. 925-939 ◽  
Author(s):  
Young-Kyo Seo ◽  
Nooshin Mirkheshti ◽  
Chung S. Song ◽  
Soyoung Kim ◽  
Sherry Dodds ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Vitamin D ◽  
Cancer Cells ◽  
Vitamin D Receptor ◽  
Tumor Tissue ◽  
Tissue Array ◽  
Cancer Tissue ◽  
Prostate Cancer Cells ◽  
Androgen Synthesis ◽  
Mouse Prostate

Abstract An elevated tumor tissue androgen level, which reactivates androgen receptor in recurrent prostate cancer, arises from the intratumor synthesis of 5α-dihydrotestosterone through use of the precursor steroid dehydroepiandrosterone (DHEA) and is fueled by the steroidogenic enzymes 3β-hydroxysteroid dehydrogenase (3β-HSD1), aldoketoreductase (AKR1C3), and steroid 5-alpha reductase, type 1 (SRD5A1) present in cancer tissue. Sulfotransferase 2B1b (SULT2B1b) (in short, SULT2B) is a prostate-expressed hydroxysteroid SULT that converts cholesterol, oxysterols, and DHEA to 3β-sulfates. DHEA metabolism involving sulfonation by SULT2B can potentially interfere with intraprostate androgen synthesis due to reduction of free DHEA pool and, thus, conversion of DHEA to androstenedione. Here we report that in prostatectomy specimens from treatment-naive patients, SULT2B expression is markedly reduced in malignant tissue (P < .001, Mann-Whitney U test) compared with robust expression in adjacent nonmalignant glands. SULT2B was detected in formalin-fixed specimens by immunohistochemistry on individual sections and tissue array. Immunoblotting of protein lysates of frozen cancer and matched benign tissue confirmed immunohistochemistry results. An in-house–developed rabbit polyclonal antibody against full-length human SULT2B was validated for specificity and used in the analyses. Ligand-activated vitamin D receptor induced the SULT2B1 promoter in vivo in mouse prostate and increased SULT2B mRNA and protein levels in vitro in prostate cancer cells. A vitamin D receptor/retinoid X receptor-α–bound DNA element (with a DR7 motif) mediated induction of the transfected SULT2B1 promoter in calcitriol-treated cells. SULT2B knockdown caused an increased proliferation rate of prostate cancer cells upon stimulation by DHEA. These results suggest that the tumor tissue SULT2B level may partly control prostate cancer growth, and its induction in a therapeutic setting may inhibit disease progression.

Effect of Obese and Lean Zucker Rat Sera on Human and Rat Prostate Cancer Cells: Implications in Obesity-Related Prostate Tumor Biology

Urology ◽  
2007 ◽  
Vol 69 (1) ◽  
pp. 191-195 ◽  
Author(s):  
Neil S. Lamarre ◽  
Michael R. Ruggieri ◽  
Alan S. Braverman ◽  
Matthew I. Gerstein ◽  
Jack H. Mydlo
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Tumor Biology ◽  
Prostate Tumor ◽  
Zucker Rat ◽  
Prostate Cancer Cells ◽  
Rat Prostate

scholarly journals Istaroxime Inhibits Motility and Down-Regulates Orai1 Expression, SOCE and FAK Phosphorylation in Prostate Cancer Cells

2017 ◽  
Vol 42 (4) ◽  
pp. 1366-1376 ◽  
Author(s):  
Matias Julian Stagno ◽  
Nefeli Zacharopoulou ◽  
Jonas Bochem ◽  
Anna Tsapara ◽  
Lisann Pelzl ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Migration ◽  
Cancer Cells ◽  
Tumor Cells ◽  
Enzyme Inhibitor ◽  
Specific Inhibitor ◽  
Prostate Tumor ◽  
Cancer Drug ◽  
Prostate Cancer Cells ◽  
Prostate Tumor Cells

Background/Aims: Istaroxime is a validated inotropic Na+/K+ ATPase inhibitor currently in development for the treatment of various cardiac conditions. Recent findings established that this steroidal drug exhibits potent apoptotic responses in prostate tumors in vitro and in vivo, by affecting key signaling orchestrating proliferation and apoptosis, such as c-Myc and caspase 3, Rho GTPases and actin cytoskeleton dynamics. In the present study we examined whether istaroxime is affecting cell motility and analyzed the underlying mechanism in prostate tumor cells. Methods: Migration was assessed by transwell and wound healing assays, Orai1 and Stim1 abundance by RT-PCR and confocal immunofluorescence microscopy, Fura-2 fluorescence was utilized to determine intracellular Ca2+ and Western blotting for FAK/pFAK measurements. Results: We observed strong inhibition of cell migration in istaroxime treated DU-145 prostate cancer cells. Istaroxime further decreased Orai1 and Stim1 transcript levels and downregulated Orai1 protein expression. Moreover, SOCE was significantly decreased upon istaroxime treatment. Furthermore, istaroxime strikingly diminished phosphorylated FAK levels. Interestingly, the efficacy of istaroxime on the inhibition of DU-145 cell migration was further enhanced by blocking Orai1 with 2-APB and FAK with the specific inhibitor PF-00562271. These results provide strong evidence that istaroxime prevents cell migration and motility of DU-145 prostate tumor cells, an effect at least partially attributed to Orai1 downregulation and FAK de-activation. Conclusion: Collectively our results indicate that this enzyme inhibitor, besides its pro-apoptotic action, affects motility of cancer cells, supporting its potential role as a strong candidate for further clinical cancer drug development.

scholarly journals Unexpected paracrine action of prostate cancer cells harboring a new class of androgen receptor mutation—A new paradigm for cooperation among prostate tumor cells

2007 ◽  
Vol 121 (6) ◽  
pp. 1238-1244 ◽  
Author(s):  
Gaëlle Lapouge ◽  
Eva Erdmann ◽  
Gemma Marcias ◽  
Monika Jagla ◽  
Audrey Monge ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Androgen Receptor ◽  
Cancer Cells ◽  
Tumor Cells ◽  
Prostate Tumor ◽  
Prostate Cancer Cells ◽  
New Paradigm ◽  
New Class ◽  
Paracrine Action ◽  
Prostate Tumor Cells
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