Expression of multidrug resistance proteins in prostate cancer is related with cell sensitivity to chemotherapeutic drugs

The Prostate ◽  
2009 ◽  
Vol 69 (13) ◽  
pp. 1448-1459 ◽  
Author(s):  
Catherine Sánchez ◽  
Patricia Mendoza ◽  
Héctor R. Contreras ◽  
Jorge Vergara ◽  
James A. McCubrey ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Multidrug Resistance ◽  
Chemotherapeutic Drugs ◽  
Multidrug Resistance Proteins ◽  
Cell Sensitivity ◽  
Resistance Proteins

scholarly journals The Emerging Role of Extracellular Vesicle-Mediated Drug Resistance in Cancers: Implications in Advanced Prostate Cancer

2015 ◽  
Vol 2015 ◽  
pp. 1-13 ◽  
Author(s):  
Carolina Soekmadji ◽  
Colleen C. Nelson
Keyword(s):  
Prostate Cancer ◽  
Drug Resistance ◽  
Multidrug Resistance ◽  
Advanced Prostate Cancer ◽  
Control Cell ◽  
Extracellular Vesicle ◽  
Multidrug Resistance Proteins ◽  
Acquired Drug Resistance ◽  
Resistance Proteins

Emerging evidence has shown that the extracellular vesicles (EVs) regulate various biological processes and can control cell proliferation and survival, as well as being involved in normal cell development and diseases such as cancers. In cancer treatment, development of acquired drug resistance phenotype is a serious issue. Recently it has been shown that the presence of multidrug resistance proteins such as Pgp-1 and enrichment of the lipid ceramide in EVs could have a role in mediating drug resistance. EVs could also mediate multidrug resistance through uptake of drugs in vesicles and thus limit the bioavailability of drugs to treat cancer cells. In this review, we discussed the emerging evidence of the role EVs play in mediating drug resistance in cancers and in particular the role of EVs mediating drug resistance in advanced prostate cancer. The role of EV-associated multidrug resistance proteins, miRNA, mRNA, and lipid as well as the potential interaction(s) among these factors was probed. Lastly, we provide an overview of the current available treatments for advanced prostate cancer, considering where EVs may mediate the development of resistance against these drugs.

Chemotherapy sensitivity recovery of prostate cancer cells by functional inhibition and knock down of multidrug resistance proteins

The Prostate ◽  
2011 ◽  
Vol 71 (16) ◽  
pp. 1810-1817 ◽  
Author(s):  
Catherine Sánchez ◽  
Alejandro Mercado ◽  
Héctor R. Contreras ◽  
Patricia Mendoza ◽  
Juan Cabezas ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Multidrug Resistance ◽  
Cancer Cells ◽  
Multidrug Resistance Proteins ◽  
Prostate Cancer Cells ◽  
Chemotherapy Sensitivity ◽  
Resistance Proteins ◽  
Knock Down ◽  
Functional Inhibition

Expression and localization of the multidrug resistance proteins MRP2 and MRP3 in human gallbladder epithelia

2001 ◽  
Vol 120 (5) ◽  
pp. A93-A93
Author(s):  
D ROST ◽  
J KONIG ◽  
G WEISS ◽  
E KLAR ◽  
W STREMMEL ◽  
...  
Keyword(s):  
Multidrug Resistance ◽  
Multidrug Resistance Proteins ◽  
Human Gallbladder ◽  
Resistance Proteins

Interaction of ivermectin with multidrug resistance proteins (MRP1, 2 and 3)

2006 ◽  
Vol 159 (3) ◽  
pp. 169-179 ◽  
Author(s):  
Anne Lespine ◽  
Jacques Dupuy ◽  
Stéphane Orlowski ◽  
Tünde Nagy ◽  
Hristos Glavinas ◽  
...  
Keyword(s):  
Multidrug Resistance ◽  
Multidrug Resistance Proteins ◽  
Resistance Proteins

Kinetics of the multidrug transporter (P-glycoprotein) and its reversal

1997 ◽  
Vol 77 (2) ◽  
pp. 545-590 ◽  
Author(s):  
W. D. Stein
Keyword(s):  
Final Section ◽  
Transport Kinetics ◽  
Multidrug Transporter ◽  
Chemotherapeutic Drugs ◽  
Multidrug Resistance Proteins ◽  
Binding Properties ◽  
Membrane Pump ◽  
Resistance Proteins ◽  
P Glycoprotein ◽  
Kinetics Of

Most cancer deaths result from the cancer's either being intrinsically resistant to chemotherapeutic drugs or becoming resistant after being initially sensitive. Often, in cells grown in cell culture, drug resistance correlates with the presence of one or more of the so-called P-glycoproteins or multidrug resistance proteins, products of the mdr family of genes. This review is largely concerned with the transport kinetics of the P-glycoproteins. We first present a brief overview of the P-glycoproteins, their properties, and their clinical significance. Later sections of the review expand on this material with special emphasis on the substrates of P-glycoprotein and how they cross the cell membrane, on the transport kinetics of the P-glycoprotein, on reversers of its action, and on its activity as an ATPase. In a final section, we consider the mechanism of action of P-glycoprotein as an actively transporting membrane pump. The characteristic of P-glycoprotein considered the most difficult to explain is its very broad specificity (or lack of specificity), but there are precedents for this property in well-known proteins such as serum albumin, which binds a range of molecular types, including substrates and reversers of P-glycoprotein, seemingly as broad as does P-glycoprotein. Pointing out this analogy does not provide a molecular explanation for the substrate-binding properties of P-glycoprotein but does make those properties more assimilable.

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