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

Sánchez, Catherine; Mendoza, Patricia; Contreras, Héctor R.; Vergara, Jorge Iván; McCubrey, James A.; Huidobro, Christian; Castellón, Enrique A.

doi:10.1002/pros.20991

Cited by 78 publications

(78 citation statements)

References 32 publications

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“…64 On the other hand, BRCP was shown to be expressed in both cell lines, while MRP-2 was only found in PC3 cells. 65,66 One possible explanation for the increased cytotoxicity following the combination treatment, despite the redundancy of the proteins targeted, is that the small TKIs are also known inhibitors of these efflux pumps.…”

mentioning

confidence: 94%

A combination of sorafenib and nilotinib reduces the growth of castrate-resistant prostate cancer

Archibald

Pritchard

Nehoff

et al. 2016

IJN

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Castrate-resistant prostate cancer (CRPC) remains incurable due to the lack of effective therapies. Several tyrosine kinases have been implicated in the development and growth of CRPC, as such targeting these kinases may offer an alternative therapeutic strategy. We established the combination of two tyrosine kinase inhibitors (TKIs), sorafenib and nilotinib, as the most cytotoxic. In addtion, to improve their bioavailability and reduce their metabolism, we encapsulated sorafenib and nilotinib into styrene- co -maleic acid micelles. The micelles’ charge, size, and release rate were characterized. We assessed the effect of the combination on the cytotoxicity, cell cycle, apoptosis, protein expression, tumor spheroid integrity, migration, and invasion. The micelles exhibited a mean diameter of 100 nm, a neutral charge, and appeared highly stable. The micellar TKIs promoted greater cytotoxicity, decreased cell proliferation, and increased apoptosis relative to the free TKIs. In addition, the combination reduced the expression and activity of several tyrosine kinases and reduced tumor spheroid integrity and metastatic potential of CRPC cell lines more efficiently than the single treatments. The combination increased the therapeutic potential and demonstrated the relevance of a targeted combination therapy for the treatment of CRPC. In addition, the efficacy of the encapsulated drugs provides the basis for an in vivo preclinical testing.

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mentioning

confidence: 94%

A combination of sorafenib and nilotinib reduces the growth of castrate-resistant prostate cancer

Archibald

Pritchard

Nehoff

et al. 2016

IJN

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“…Chemoresistant PC3 cells do not overexpress P-gp, whereas resistant DU145 cells exhibit both overexpression of the protein and restored chemo-sensitivity with P-gp inhibition (Makarovskiy et al 2002, Takeda et al 2007. Furthermore, exposure to mitoxantrone and docetaxel results in increased multidrug-resistant protein expression in chemo-sensitive prostate cancer cell lines (Sanchez et al 2009). Although MDR1 is well understood, MRP1 is also emerging as an important element in prostate cancer chemoresistance (Zalcberg et al 2000.…”

Section: Multidrug Resistance Proteinsmentioning

confidence: 99%

Pathways of chemotherapy resistance in castration-resistant prostate cancer

Mahon¹,

Henshall²,

Sutherland³

et al. 2011

Endocrine-Related Cancer

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Chemotherapy remains the major treatment option for castration-resistant prostate cancer (CRPC) and limited cytotoxic options are available. Inherent chemotherapy resistance occurs in half of all patients and inevitably develops even in those who initially respond. Docetaxel has been the mainstay of therapy for 6 years, providing a small survival benefit at the cost of significant toxicity. Cabazitaxel is a promising second-line agent; however, it is no less toxic, whereas mitoxantrone provides only symptomatic benefit. Multiple cellular pathways involving apoptosis, inflammation, angiogenesis, signalling intermediaries, drug efflux pumps and tubulin are implicated in the development of chemoresistance. A thorough understanding of these pathways is needed to identify biomarkers that predict chemotherapy resistance with the aim to avoid unwarranted toxicities in patients who will not benefit from treatment. Until recently, the search for predictive biomarkers has been disappointing; however, the recent discovery of macrophage inhibitory cytokine 1 as a marker of chemoresistance may herald a new era of biomarker discovery in CRPC. Understanding the interface between this complex array of chemoresistance pathways rather than their study in isolation will be required to effectively predict response and target the late stages of advanced disease. The pre-clinical evidence for these resistance pathways and their progress through clinical trials as therapeutic targets is reviewed in this study.

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“…Previous studies have demonstrated that MDR1 is an important candidate gene in the pathogenesis of osteoporosis (van Brussel and Mickisch, 2003;Sanchez et al, 2009;Sanchez et al, 2011). To the best of our knowledge, the current study is the first to investigate the prevalence of the c.1465C>T variant, which is located in exon14 of MDR1, and evaluate its relationship with Pca risk.…”

Section: Discussionmentioning

confidence: 87%

“…The pathogenesis of Pca is still largely unknown, with genetic and environmental factors likely contributing to increased risk of the disease (Pienta and Esper 1993;Lichtenstein et al, 2000;Schaid, 2004). Several candidate genes have been suggested to be associated with Pca, including multidrug resistance 1 (MDR1) (van Brussel and Mickisch, 2003;Sanchez et al, 2009;Sanchez et al, 2011), X-ray repair complementing group 1 (Hirata et al, 2007;Agalliu et al, 2010;Dhillon et al, 2011;Kuasne et al, 2011;Langsenlehner et al, 2011), xeroderma pigmentosum group D gene (Mandal et al, 2010), APEX nuclease 1 gene (Agalliu et al, 2010;Kuasne et al, 2011;Mittal et al, 2012), Toll-like receptor 4 (Jing et al, 2012), axis inhibition protein 2 (Pinarbasi et al, 2011), 2-5A-dependent RNase (Wei et al, 2012), complementation group G gene (Berhane et al, 2012), and N-acetyltransferase types 1 (Gong et al, 2011) and 2 (Gong et al, 2011;de Lima Junior et al, 2012). MDR1 is an important candidate gene for Pca.…”

Section: Introductionmentioning

confidence: 99%

“…MDR1 is an important candidate gene for Pca. Evidence from previous studies has suggested that common polymorphisms in MDR1 are associated with the risk of Pca (van Brussel and Mickisch, 2003;Sanchez et al, 2009;Sanchez et al, 2011). Several MDR1 singlenucleotide polymorphisms (SNPs) such as C2677T and C3435T have been detected to affect the risk of Pca (Narter et al, 2006).…”

Section: Introductionmentioning

confidence: 99%

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Relationship between multidrug resistance 1 polymorphisms and the risk of prostate cancer in Chinese populations

Shen¹,

Yan²,

Liu³

et al. 2013

Genet. Mol. Res.

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ABSTRACT. Prostate cancer is one of the most common malignancies in men. The multidrug resistance 1 gene (MDR1) is an important candidate gene for prostate cancer. The aim of this study was to evaluate the association between MDR1 gene polymorphisms and the risk of prostate cancer. MDR1 gene polymorphism and its association with the risk of prostate cancer were investigated in 357 Chinese men. A novel c.1465C>T polymorphism was detected with created restriction site-polymerase chain reaction and DNA sequencing. We found a significantly increased risk of prostate cancer in the homozygote comparison [TT vs CC: odds ratio (OR) = 2.300,

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

Cited by 78 publications

References 32 publications

A combination of sorafenib and nilotinib reduces the growth of castrate-resistant prostate cancer

A combination of sorafenib and nilotinib reduces the growth of castrate-resistant prostate cancer

Pathways of chemotherapy resistance in castration-resistant prostate cancer

Relationship between multidrug resistance 1 polymorphisms and the risk of prostate cancer in Chinese populations

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