Nano-based strategies to overcome p-glycoprotein-mediated drug resistance

Niazi, Mehri; Zakeri–Milani, Parvin; Hajivar, Saeedeh Najafi; Soleymani-Goloujeh, Mehdi; Ghobakhlou, Nasrin; Mojarrad, Javid Shahbazi; Valizadeh, Hadi

doi:10.1080/17425255.2016.1196186

Cited by 42 publications

(31 citation statements)

References 116 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Beyond chemical modification of a drug, advances in other technologies are also looking promising. For example nanoparticle delivery systems to allow better targeting or addressing specific molecular alterations in resistant tumours [73]. It may also be possible to develop multifunctional nanoparticles able to simultaneously target multiple resistance mechanisms.…”

Section: Use Of Multiple Mechanismsmentioning

confidence: 99%

Molecular chess? Hallmarks of anti-cancer drug resistance

2017

View full text Add to dashboard Cite

BackgroundThe development of resistance is a problem shared by both classical chemotherapy and targeted therapy. Patients may respond well at first, but relapse is inevitable for many cancer patients, despite many improvements in drugs and their use over the last 40 years.ReviewResistance to anti-cancer drugs can be acquired by several mechanisms within neoplastic cells, defined as (1) alteration of drug targets, (2) expression of drug pumps, (3) expression of detoxification mechanisms, (4) reduced susceptibility to apoptosis, (5) increased ability to repair DNA damage, and (6) altered proliferation. It is clear, however, that changes in stroma and tumour microenvironment, and local immunity can also contribute to the development of resistance. Cancer cells can and do use several of these mechanisms at one time, and there is considerable heterogeneity between tumours, necessitating an individualised approach to cancer treatment. As tumours are heterogeneous, positive selection of a drug-resistant population could help drive resistance, although acquired resistance cannot simply be viewed as overgrowth of a resistant cancer cell population. The development of such resistance mechanisms can be predicted from pre-existing genomic and proteomic profiles, and there are increasingly sophisticated methods to measure and then tackle these mechanisms in patients.ConclusionThe oncologist is now required to be at least one step ahead of the cancer, a process that can be likened to ‘molecular chess’. Thus, as well as an increasing role for predictive biomarkers to clinically stratify patients, it is becoming clear that personalised strategies are required to obtain best results.

show abstract

Section: Use Of Multiple Mechanismsmentioning

confidence: 99%

Molecular chess? Hallmarks of anti-cancer drug resistance

2017

View full text Add to dashboard Cite

show abstract

“…Pglycoprotein (P-gp) membrane proteins are encoded by MDR gene family; which is well known as ABC transporters (153). P-gp effluxes hydrophobic and positively charged xenobiotics like DOX and paclitaxel out of the cells; and reduce the chemotherapy efficiency (154)(155)(156). D188 (Aspartic acid in the position 188), E353 (Glutamic acid in the position 353), E782, and D997 are residues close to the membrane surface and are located outside the perimeter of the intracellular domain helices of P-gp inside the chamber.…”

Section: Importance Of Zp In Overcoming Multidrug Resistance In Cancementioning

confidence: 99%

Drug Targeting Strategies Based on Charge Dependent Uptake of Nanoparticles into Cancer Cells

et al. 2019

Self Cite

View full text Add to dashboard Cite

The aim of this review was to describe the preferred charged nano-particles (CNPs) for targeted delivery in tumor cells. Zeta Potential (ZP), which represents the surface charge of NPs was highlighted in cell entrance and interactions. In this regard, various types of endocytosis pathways which are involved in NPs’ uptake were first introduced. Then, significance of positively charged NPs (PCNPs) in proton sponge effect corresponding to lysosomal escape was discussed. Cells prefer to endocyte the NPs with positive charge in passive targeting and gene delivery, while in active targeting; the charge of receptors’ ligand binding site determines the NPs cellular uptake. Moreover, pH-sensitive NPs represent charge reversible behavior depending on pH changes which leads to longer blood circulation residence and higher uptake at acidic microenvironment of the cancer media. Role of the CNPs in overcoming multidrug resistance (MDR) and bypassing p-glycoprotein was further investigated.

show abstract

“…In the efforts to combat MDR, nanoparticles (NPs) composed of gold, silver, or titanium dioxide (TiO 2 ) are thought to be one of the most promising strategies, as they can accumulate specifically and rapidly in cancer cells by enhanced permeability and retention effects (Niazi et al, ; Yin, Deng, Zhang, & Lin, ). More importantly, nano‐sized medicines enter cancer cells by endocytic pathways, therefore circumventing the efflux of transporters (Li et al, ).…”

Section: Introductionmentioning

confidence: 99%

MicroRNA‐mediated suppression of P‐glycoprotein by quantum dots in lung cancer cells

Sun

Zhang

Yin

et al. 2019

J of Applied Toxicology

View full text Add to dashboard Cite

The interactions between adenosine triphosphate‐binding cassette (ABC) transporters and nano‐sized materials are attracting increasing attention, due to their great potential in overcoming the multidrug resistance (MDR) phenomena in cancer treatment. However, the inner mechanisms involved in the interactions are largely unknown. In this study, two commercial quantum dots (QDs), CdSe/ZnS‐MPA and CdSe/ZnS‐GSH, were tested for their interactions with P‐glycoprotein (P‐gp), as well as the relating mechanisms in lung cancer (A549) cells. Both QDs significantly suppressed the gene and protein expressions of P‐gp in A549 cells. To explain this, the gene expressions of nine relating microRNAs (miRNAs) were evaluated. The results indicated a shared up‐regulation of miR‐34b and miR‐185 by both QDs. Furthermore, mimics and inhibitors of miR‐34b and miR‐185 significantly enhanced and suppressed the gene and protein expressions of P‐gp, respectively, confirming the modulatory function of these two miRNAs on P‐gp. Interestingly, expressions of both miRNAs were suppressed during treatment with Cd2+ and doxorubicin, which induced the expression of P‐gp, indicating the universality of these miRNAs‐related mechanisms. Thus, as miR‐34b and miR‐185 participated in the suppression of P‐gp functions in A549 cells they could be interesting targets for the treatment of lung cancer.

show abstract

Nano-based strategies to overcome p-glycoprotein-mediated drug resistance

Cited by 42 publications

References 116 publications

Molecular chess? Hallmarks of anti-cancer drug resistance

Molecular chess? Hallmarks of anti-cancer drug resistance

Drug Targeting Strategies Based on Charge Dependent Uptake of Nanoparticles into Cancer Cells

MicroRNA‐mediated suppression of P‐glycoprotein by quantum dots in lung cancer cells

Contact Info

Product

Resources

About