The association of Id-1, MIF and GSTpi with acquired drug resistance in hormone independent prostate cancer cells

2005 ◽  
Author(s):  
Jau-Chen Lin ◽  
Sun-Yran Chang ◽  
Dar-Shih Hsieh ◽  
Chi-Feng Lee ◽  
Dah-Shyong Yu
Keyword(s):  
Prostate Cancer ◽  
Drug Resistance ◽  
Cancer Cells ◽  
Prostate Cancer Cells ◽  
Acquired Drug Resistance

scholarly journals Acidosis induces multi-drug resistance in rat prostate cancer cells (AT1)in vitroandin vivoby increasing the activity of the p-glycoproteinviaactivation of p38

2008 ◽  
Vol 123 (11) ◽  
pp. 2532-2542 ◽  
Author(s):  
Christoph Sauvant ◽  
Martin Nowak ◽  
Claudia Wirth ◽  
Bettina Schneider ◽  
Anne Riemann ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Drug Resistance ◽  
Cancer Cells ◽  
Multi Drug Resistance ◽  
Prostate Cancer Cells ◽  
Rat Prostate

Docetaxel-ST1481 sequence exerts a potent cytotoxic activity on hormone-resistant prostate cancer cells by reducing drug resistance-related gene expression

The Prostate ◽  
2009 ◽  
Vol 70 (2) ◽  
pp. 219-227 ◽  
Author(s):  
Francesco Fabbri ◽  
Giovanni Brigliadori ◽  
Silvia Carloni ◽  
Paola Ulivi ◽  
Anna Tesei ◽  
...  
Keyword(s):  
Gene Expression ◽  
Prostate Cancer ◽  
Drug Resistance ◽  
Cytotoxic Activity ◽  
Cancer Cells ◽  
Related Gene ◽  
Prostate Cancer Cells ◽  
Hormone Resistant Prostate Cancer

scholarly journals PO-235 Fenofibrate overcomes the drug-resistance of human prostate cancer cells

2018 ◽  
Author(s):  
M Luty ◽  
K Piwowarczyk ◽  
T Wróbel ◽  
D Ryszawy ◽  
A Łabędź-MasŁowska ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Drug Resistance ◽  
Cancer Cells ◽  
Human Prostate ◽  
Human Prostate Cancer ◽  
Prostate Cancer Cells

scholarly journals Expression of Androgen Receptor Variant 7 (AR-V7) in Circulated Tumor Cells and Correlation with Drug Resistance of Prostate Cancer Cells

2018 ◽  
Vol 24 ◽  
pp. 7051-7056 ◽  
Author(s):  
Shuaibin Wang ◽  
Sen Yang ◽  
Cunjin Nan ◽  
Yijun Wang ◽  
Youhua He ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Drug Resistance ◽  
Androgen Receptor ◽  
Cancer Cells ◽  
Tumor Cells ◽  
Prostate Cancer Cells

scholarly journals Metabolic Reprogramming and Predominance of Solute Carrier Genes during Acquired Enzalutamide Resistance in Prostate Cancer

Cells ◽  
2020 ◽  
Vol 9 (12) ◽  
pp. 2535
Author(s):  
Shiv Verma ◽  
Eswar Shankar ◽  
E. Ricky Chan ◽  
Sanjay Gupta
Keyword(s):  
Prostate Cancer ◽  
Drug Resistance ◽  
Cancer Cells ◽  
Standard Of Care ◽  
Resistant Cell ◽  
Metabolic Reprogramming ◽  
Differentially Expressed ◽  
Pcr Analysis ◽  
Prostate Cancer Cells ◽  
Solute Carrier

Androgen deprivation therapy (ADT) is standard-of-care for advanced-stage prostate cancer, and enzalutamide (Xtandi®, Astellas, Northbrook, IL, USA), a second generation antiandrogen, is prescribed in this clinical setting. The response to this medication is usually temporary with the rapid emergence of drug resistance. A better understanding of gene expression changes associated with enzalutamide resistance will facilitate circumventing this problem. We compared the transcriptomic profile of paired enzalutamide-sensitive and resistant LNCaP and C4-2B prostate cancer cells for identification of genes involved in drug resistance by performing an unbiased bioinformatics analysis and further validation. Next-Gen sequencing detected 9409 and 7757 genes differentially expressed in LNCaP and C4-2B cells, compared to their parental counterparts. A subset of differentially expressed genes were validated by qRT-PCR. Analysis by the i-pathway revealed membrane transporters including solute carrier proteins, ATP-binding cassette transporters, and drug metabolizing enzymes as the most prominent genes dysregulated in resistant cell lines. RNA-Seq data demonstrated predominance of solute carrier genes SLC12A5, SLC25A17, and SLC27A6 during metabolic reprogramming and development of drug resistance. Upregulation of these genes were associated with higher uptake of lactic/citric acid and lower glucose intake in resistant cells. Our data suggest the predominance of solute carrier genes during metabolic reprogramming of prostate cancer cells in an androgen-deprived environment, thus signifying them as potentially attractive therapeutic targets.

Oncogene overexpression and de novo drug-resistance in human prostate cancer cells

1994 ◽  
Vol 1226 (1) ◽  
pp. 89-96 ◽  
Author(s):  
Hiroyuki Yamazaki ◽  
Erasmus Schneider ◽  
Charles E. Myers ◽  
Birandra K. Sinha
Keyword(s):  
Prostate Cancer ◽  
Drug Resistance ◽  
Cancer Cells ◽  
De Novo ◽  
Human Prostate ◽  
Human Prostate Cancer ◽  
Prostate Cancer Cells

991 APE1/REF-1 REGULATES SURVIVIN-MEDIATED DRUG RESISTANCE IN PROSTATE CANCER CELLS

2013 ◽  
Vol 189 (4S) ◽  
Author(s):  
David McIlwain ◽  
Melissa Fishel ◽  
Liang Wang ◽  
Brandy Snider ◽  
Jian-Ting Zhang ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Drug Resistance ◽  
Cancer Cells ◽  
Prostate Cancer Cells

scholarly journals Fenofibrate Augments the Sensitivity of Drug-Resistant Prostate Cancer Cells to Docetaxel

Cancers ◽  
2019 ◽  
Vol 11 (1) ◽  
pp. 77
Author(s):  
Marcin Luty ◽  
Katarzyna Piwowarczyk ◽  
Anna Łabędź-Masłowska ◽  
Tomasz Wróbel ◽  
Małgorzata Szczygieł ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Drug Resistance ◽  
Cancer Cells ◽  
Combined Treatment ◽  
Metronomic Chemotherapy ◽  
Drug Resistant ◽  
Prostate Cancer Cells ◽  
Pc3 Cells ◽  
Effective Doses ◽  
Resistant Cells

Metronomic agents reduce the effective doses and adverse effects of cytostatics in cancer chemotherapy. Therefore, they can enhance the treatment efficiency of drug-resistant cancers. Cytostatic and anti-angiogenic effects of fenofibrate (FF) suggest that it can be used for the metronomic chemotherapy of drug-resistant prostate tumors. To estimate the effect of FF on the drug-resistance of prostate cancer cells, we compared the reactions of naïve and drug-resistant cells to the combined treatment with docetaxel (DCX)/mitoxantrone (MTX) and FF. FF sensitized drug-resistant DU145 and PC3 cells to DCX and MTX, as illustrated by their reduced viability and invasive potential observed in the presence of DCX/MTX and FF. The synergy of the cytostatic activities of both agents was accompanied by the inactivation of P-gp-dependent efflux, dysfunction of the microtubular system, and induction of polyploidy in DCX-resistant cells. Chemical inhibition of PPARα- and reactive oxygen species (ROS)-dependent pathways by GW6471 and N-acetyl-L-cysteine, respectively, had no effect on cell sensitivity to combined DCX/FF treatment. Instead, we observed the signs of adenosine triphosphate (ATP) deficit and autophagy in DCX/FF-treated drug-resistant cells. Furthermore, the cells that had been permanently propagated under DCX- and DCX/FF-induced stress did not acquire DCX/FF-resistance. Instead, relatively slow proliferation of DCX-resistant cells was efficiently inhibited by FF. Collectively, our observations show that FF reduces the effective doses of DCX by interfering with the drug resistance and energy metabolism of prostate cancer cells. Concomitantly, it impairs the chemotherapy-induced microevolution and expansion of DCX/FF-resistant cells. Therefore, FF can be applied as a metronomic agent to enhance the efficiency of palliative chemotherapy of prostate cancer.

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