scholarly journals Radiosensitization by the investigational NEDD8-activating enzyme inhibitor MLN4924 (pevonedistat) in hormone-resistant prostate cancer cells

Oncotarget ◽  
2016 ◽  
Vol 7 (25) ◽  
pp. 38380-38391 ◽  
Author(s):  
Xiaofang Wang ◽  
Wenjuan Zhang ◽  
Zi Yan ◽  
Yupei Liang ◽  
Lihui Li ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Enzyme Inhibitor ◽  
Prostate Cancer Cells ◽  
Hormone Resistant Prostate Cancer

scholarly journals Identification of a Radiosensitivity Molecular Signature Induced by Enzalutamide in Hormone-sensitive and Hormone-resistant Prostate Cancer Cells

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Maryam Ghashghaei ◽  
Tamim M. Niazi ◽  
Adriana Aguilar-Mahecha ◽  
Kathleen Oros Klein ◽  
Celia M. T. Greenwood ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Molecular Signature ◽  
Prostate Cancer Cells ◽  
Hormone Sensitive ◽  
Hormone Resistant Prostate Cancer

Induction of Fas clustering and apoptosis by coral prostanoid in human hormone-resistant prostate cancer cells

2006 ◽  
Vol 542 (1-3) ◽  
pp. 22-30 ◽  
Author(s):  
Po-Cheng Chiang ◽  
Fan-Lu Kung ◽  
Dong-Ming Huang ◽  
Tsai-Kun Li ◽  
Jia-Rong Fan ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Prostate Cancer Cells ◽  
Hormone Resistant Prostate Cancer

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.

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