Intelligent micro-vehicles for drug transport and controlled release to cancer cells

2021 ◽  
pp. 104961
Author(s):  
Marieta Constantin ◽  
Sanda Bucatariu ◽  
Irina Popescu ◽  
Bogdan Cosman ◽  
Paolo Ascenzi ◽  
...  
Keyword(s):  
Controlled Release ◽  
Cancer Cells ◽  
Drug Transport

scholarly journals pH and redox dual-sensitive drug delivery system constructed based on fluorescent carbon dots

RSC Advances ◽  
2021 ◽  
Vol 11 (5) ◽  
pp. 2656-2663
Author(s):  
Boye Zhang ◽  
Qianqian Duan ◽  
Yi Li ◽  
Jianming Wang ◽  
Wendong Zhang ◽  
...  
Keyword(s):  
Drug Delivery ◽  
Controlled Release ◽  
Cancer Cells ◽  
Fluorescence Imaging ◽  
Drug Delivery System ◽  
Delivery System ◽  
Carbon Dots ◽  
Ph Responsive ◽  
Charge Reversal ◽  
Fluorescent Carbon Dots

The system is pH-responsive and redox-controlled release. And the charge reversal and size transitions of the system can enhance the targeted ability. Moreover, the system can recognize the cancer cells by the fluorescence imaging.

Targeting cancer cells with controlled release nanocapsules based on a single aptamer

2013 ◽  
Vol 49 (13) ◽  
pp. 1285 ◽  
Author(s):  
Frank J. Hernandez ◽  
Luiza I. Hernandez ◽  
Alessandro Pinto ◽  
Thomas Schäfer ◽  
Veli C. Özalp
Keyword(s):  
Controlled Release ◽  
Cancer Cells

Oxime-based 19-nortestosterone–pheophorbide a conjugate: bimodal controlled release concept for PDT

2019 ◽  
Vol 7 (36) ◽  
pp. 5465-5477 ◽  
Author(s):  
Vladimíra Pavlíčková ◽  
Michal Jurášek ◽  
Silvie Rimpelová ◽  
Kamil Záruba ◽  
David Sedlák ◽  
...  
Keyword(s):  
Photodynamic Therapy ◽  
Androgen Receptor ◽  
Controlled Release ◽  
Cancer Cells ◽  
Pheophorbide A

Nandrolone–pheophorbide a fluorescent conjugate exhibiting promising potential in targeting of androgen receptor-positive cancer cells and their destruction by photodynamic therapy.

Triblock Copolymer Nanovesicles for pH-Responsive Targeted Delivery and Controlled Release of siRNA to Cancer Cells

2015 ◽  
Vol 16 (7) ◽  
pp. 1924-1937 ◽  
Author(s):  
Elena Gallon ◽  
Teresa Matini ◽  
Luana Sasso ◽  
Giuseppe Mantovani ◽  
Ana Armiñan de Benito ◽  
...  
Keyword(s):  
Controlled Release ◽  
Cancer Cells ◽  
Targeted Delivery ◽  
Triblock Copolymer ◽  
Ph Responsive

scholarly journals The Selective Class IIa Histone Deacetylase Inhibitor TMP195 Resensitizes ABCB1- and ABCG2-Overexpressing Multidrug-Resistant Cancer Cells to Cytotoxic Anticancer Drugs

2019 ◽  
Vol 21 (1) ◽  
pp. 238 ◽  
Author(s):  
Chung-Pu Wu ◽  
Sabrina Lusvarghi ◽  
Jyun-Cheng Wang ◽  
Sung-Han Hsiao ◽  
Yang-Hui Huang ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Histone Deacetylase ◽  
Anticancer Drugs ◽  
Drug Transport ◽  
Drug Repurposing ◽  
Binding Pocket ◽  
Multidrug Resistant ◽  
Drug Induced ◽  
In Silico Docking

Multidrug resistance caused by the overexpression of the ATP-binding cassette (ABC) proteins in cancer cells remains one of the most difficult challenges faced by drug developers and clinical scientists. The emergence of multidrug-resistant cancers has driven efforts from researchers to develop innovative strategies to improve therapeutic outcomes. Based on the drug repurposing approach, we discovered an additional action of TMP195, a potent and selective inhibitor of class IIa histone deacetylase. We reveal that in vitro TMP195 treatment significantly enhances drug-induced apoptosis and sensitizes multidrug-resistant cancer cells overexpressing ABCB1 or ABCG2 to anticancer drugs. We demonstrate that TMP195 inhibits the drug transport function, but not the protein expression of ABCB1 and ABCG2. The interaction between TMP195 with these transporters was supported by the TMP195-stimulated ATPase activity of ABCB1 and ABCG2, and by in silico docking analysis of TMP195 binding to the substrate-binding pocket of these transporters. Furthermore, we did not find clear evidence of TMP195 resistance conferred by ABCB1 or ABCG2, suggesting that these transporters are unlikely to play a significant role in the development of resistance to TMP195 in cancer patients.

scholarly journals Enhanced antitumor activity of carbendazim on HeLa cervical cancer cells by aptamer mediated controlled release

RSC Advances ◽  
2019 ◽  
Vol 9 (62) ◽  
pp. 36005-36010
Author(s):  
Bilge G. Tuna ◽  
Pinar B. Atalay ◽  
Gamze Kuku ◽  
E. Esma Acar ◽  
H. Kubra Kara ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Controlled Release ◽  
Antitumor Activity ◽  
Mesoporous Silica ◽  
Cell Surface ◽  
Hela Cell ◽  
Cancer Cells ◽  
Mesoporous Silica Nanoparticles ◽  
Functionalized Mesoporous Silica ◽  
Cervical Cancer Cells

Carbendazim doped and aptamer-gate functionalized mesoporous silica nanoparticles targeted nucleolin on HeLa cell surface for specific delivery. This delivery system improved antitumor activity of carbendazim by about 3 folds increase of EC50 values.

scholarly journals The Second-Generation PIM Kinase Inhibitor TP-3654 Resensitizes ABCG2-Overexpressing Multidrug-Resistant Cancer Cells to Cytotoxic Anticancer Drugs

2021 ◽  
Vol 22 (17) ◽  
pp. 9440
Author(s):  
Chung-Pu Wu ◽  
Yan-Qing Li ◽  
Ya-Chen Chi ◽  
Yang-Hui Huang ◽  
Tai-Ho Hung ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Anticancer Drugs ◽  
Drug Transport ◽  
Second Generation ◽  
Kinase Inhibitor ◽  
Multidrug Resistant ◽  
Drug Efflux ◽  
Transport Function ◽  
Therapy Option ◽  
Induction Of Resistance

Human ATP-binding cassette (ABC) subfamily G member 2 (ABCG2) mediates the transport of a wide variety of conventional cytotoxic anticancer drugs and molecular targeted agents. Consequently, the overexpression of ABCG2 in cancer cells is linked to the development of the multidrug resistance (MDR) phenotype. TP-3654 is an experimental second-generation inhibitor of PIM kinase that is currently under investigation in clinical trials to treat advanced solid tumors and myelofibrosis. In this study, we discovered that by attenuating the drug transport function of ABCG2, TP-3654 resensitizes ABCG2-overexpressing multidrug-resistant cancer cells to cytotoxic ABCG2 substrate drugs topotecan, SN-38 and mitoxantrone. Moreover, our results indicate that ABCG2 does not mediate resistance to TP-3654 and may not play a major role in the induction of resistance to TP-3654 in cancer patients. Taken together, our findings reveal that TP-3654 is a selective, potent modulator of ABCG2 drug efflux function that may offer an additional combination therapy option for the treatment of multidrug-resistant cancers.

scholarly journals Controlled release of targeted anti-leukemia drugs azacitidine and decitabine monitored using surface-enhanced Raman scattering (SERS) spectroscopy

2017 ◽  
Vol 6 (4) ◽  
pp. 125-132 ◽  
Author(s):  
Madison Smith ◽  
Maria Hepel
Keyword(s):  
Drug Delivery ◽  
Folic Acid ◽  
Controlled Release ◽  
Drug Release ◽  
Raman Scattering ◽  
Cancer Cells ◽  
Surface Enhanced Raman Scattering ◽  
Surface Enhanced ◽  
Surface Enhanced Raman ◽  
Enhanced Raman Scattering

A new targeted drug delivery system with controlled release of anti-cancer drugs, azacitidine and decitabine, was investigated to enhance the efficacy of cancer treatment and reduce the effects of high drug toxicity to healthy tissues. The proposed drug nanocarriers are based on gold nanoparticles (AuNPs) modified with mercaptobenzoic acid (MBA) linker to enable the immobilization of azacitidine (AZA) and decitabine (DAC) on AuNPs in the form of AuNP@MBA/AZA,DAC entities. The cancer cell recognition was accomplished by covalently binding folic acid (FA) ligands to para-aminothiophenol (PATP) in the mixed SAM shell on gold nanoparticle nanocarriers, AuNP@MBA,PATP. The FA ligand was used due to the strong expression of folic acid receptors (FR) in the membrane of cancer cells. This enables the functionalized carriers to target only cancer cells owing to the efficient FA-FR binding property. The amide bonds between the linkers and azacitidine/decitabine are pH sensitive and undergo acid hydrolysis in a low pH environment of the cytosol in cancer cells. Using the solutions of different pH, the release of azacitidine/decitabine was monitored by surface-enhanced Raman scattering spectroscopy (SERS) measurements of the MBA Raman modes at 1586 cm-1 and 1074 cm-1 . At pH 7.4, the release of the drug was found to be negligible, while at pH 4.0 and 5.5 a continuous drug release was observed over 3 hours. The utilization of SERS monitoring for the drug release was based on the strong Raman signals which are generated by the MBA linker when it is bound to a plasmonic AuNP. During the immobilization of azacitidine/decitabine on AuNP carriers, the SERS signals are strongly reduced due to the shielding by drug molecules but they increase sharply upon the drug release confirming the amide bond breakage and successful drug delivery.

Sign in / Sign up

Export Citation Format

Share Document