scholarly journals Fabrication of psoralen-loaded lipid-polymer hybrid nanoparticles and their reversal effect on drug resistance of cancer cells

Author(s):  
Yueling Yuan ◽  
Peter Chiba ◽  
Tiange Cai ◽  
Richard Callaghan ◽  
Li Bai ◽  
...  
2018 ◽  
Vol 48 ◽  
pp. 96-105 ◽  
Author(s):  
Hannaneh monirinasab ◽  
Hamed Asadi ◽  
Kobra Rostamizadeh ◽  
Abdolreza Esmaeilzadeh ◽  
Malihe Khodaei ◽  
...  

2010 ◽  
Vol 38 (02) ◽  
pp. 401-413 ◽  
Author(s):  
Meng Xu ◽  
Liang-He Sheng ◽  
Xi-Hai Zhu ◽  
Shi-Bin Zeng ◽  
Guo-Jun Zhang

This research is aimed on reversing multidrug resistance (MDR) of chemotherapy in lung cancer. According to our previous research, chemotherapeutic drugs resistance in lung cancer is mainly due to high expression of multidrug resistance-associated protein (MRP) gene and activation of caspases. The effect of stephania tetrandra-containing Chinese herbal formula, namely Supplement Energy and Nourish Lung (SENL), is effective in enhancing efficacy and reducing toxicity of chemotherapy in lung cancer. However, the underlying mechnism is largely unknown. To understand whether and how SENL herbs function on multidrug-resistance lung cancer cells, we treated a multidrug resistance lung cancer cell line, SW1573/2R120 with SENL herbs alone or together with a chemotherapeutic drug, Adriamycin (ADM). We observed that SENL herbs had a significant synergistic effect with ADM in inhibiting the growth of SW1573/2R120 cells. SENL alone and particularly together with ADM could significantly increase cell apoptotic death via mitochondria- and caspase-dependent pathway. Furthermore, we showed that SENL herbs could reverse drug resistance of lung cancer cells by decreasing MRP expression and increasing accumulation of intracellular ADM, which in turn increase the sensitivity of cancer cells to ADM. Taken together, the mechanism underlying reversal effect of drug resistance by SENL treatment was reported here and further systematical investigation on SENL herbs may lead to solve drug resistance in lung cancer chemotherapy.


2017 ◽  
Vol 41 (4) ◽  
pp. 1518-1525 ◽  
Author(s):  
Shao-Qi Zeng ◽  
Yi-Zhen Chen ◽  
Yong Chen ◽  
Hong Liu

Co-delivery of a chemotherapeutic drug and a drug resistance inhibitor by lipid–polymer hybrid nanoparticles can effectively overcome tumor drug resistance.


Nanoscale ◽  
2017 ◽  
Vol 9 (43) ◽  
pp. 17044-17053 ◽  
Author(s):  
Wei Zhou ◽  
Hui Yu ◽  
Liu-Jie Zhang ◽  
Bo Wu ◽  
Cai-Xia Wang ◽  
...  

The mitochondria-targeting of lipid–polymer hybrid nanoparticles can be activated by a redox-signal in cancer cells for highly efficient cancer chemotherapy.


RSC Advances ◽  
2015 ◽  
Vol 5 (22) ◽  
pp. 16931-16939 ◽  
Author(s):  
Zhenbao Liu ◽  
Huanzhe Zhao ◽  
Lingyun He ◽  
Yao Yao ◽  
Yanbin Zhou ◽  
...  

In this work, MUC1 aptamer (designated S2.2) modified and vinorelbine (VRL) loaded lipid-polymer hybrid nanoparticles (Apt-VRL-NPs) were prepared.


2021 ◽  
Author(s):  
Tengteng Zou ◽  
Meng Lan ◽  
Lihong Li ◽  
Tiange Cai ◽  
Yu Cai

Abstract Background The role of epithelial mesenchymal transition (EMT) involved in breast cancer metastasis and chemoresistance has been increasingly recognized. However, it’s necessary to search for more effective strategies to inhibit EMT thereby increase the sensitivity of breast cancer cells to chemotherapy drugs. Emodin has a potential in overcoming tumor drug resistance and restraining the development of EMT, but the poor internalization into breast cancer cells limited the application. Results MCF-7/ADR cells have more EMT characteristics than MCF-7 cell. EMT in MCF-7/ADR cells promotes the development of drug resistance via apoptosis resistance and facilitating the expression of P-gp. The anti-cancer effect of DOX enhanced by the decreasing of drug resistance protein P-gp and apoptosis related proteins after EMT inhibited in MCF-7/ADR cells. E-PLNs increase the cellular uptake of EMO and restore DOX sensitivity in MCF-7/ADR cells by inhibiting EMT. Conclusion E-PLNs inhibit EMT to enhance the sensitivity of breast cancer to DOX. The combination of E-PLNs and DOX can improve the efficacy of DOX in the treatment of breast cancer, which provides a new method to prevent or delay clinical drug resistance.


2020 ◽  
Author(s):  
Ping Yang ◽  
Lian Zhang ◽  
Tian Wang ◽  
Qi Liu ◽  
Jing Wang ◽  
...  

Abstract In this study, we have prepared a novel folate receptor-targeted doxorubicin (DOX) and edelfosine (ET)-loaded lipid polymer hybrid nanoparticle to enhance the anticancer efficacy in osteosarcoma. The dual-drug loaded nanoparticles showed a nanosized morphology and physiological stability. The targeted nanoparticles showed enhanced cellular internalization and subcellular distribution in MG63 cancer cells compared to that of non-targeted nanoparticles. Among many ratios of DOX and ET, 1:1 ratiometric combinations of drugs were observed to be highly synergistic in killing the cancer cells. MTT assay and caspase-3/7 activity assay clearly showed the superior anticancer efficacy of DE-FPLN formulations in inducing the cancer cell death. In vitro results indicate that the co-administration of two drugs in a folic acid-targeted nanoparticle could potentially induce the apoptosis and cell death. In vivo results displayed the potency of tumor cell killing and significant suppression of tumor growth without any detectable side effects. The lipid polymer hybrid nanocarriers with multiple properties of high drug loading, sequential and ratiometric drug release, improved physiological stability, prolonged blood circulation, and tumor-specific targeting are promising for the delivery of multiple drugs in the treatment of osteosarcoma.


2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Tengteng Zou ◽  
Meng Lan ◽  
Fengjie Liu ◽  
Lihong Li ◽  
Tiange Cai ◽  
...  

Abstract Background The role of epithelial–mesenchymal transition (EMT) involved in breast cancer metastasis and chemoresistance has been increasingly recognized. However, it is necessary to search for more effective strategies to inhibit EMT thereby increase the sensitivity of breast cancer cells to chemotherapy drugs. Emodin has a potential in overcoming tumor drug resistance and restraining the development of EMT, but the poor internalization into breast cancer cells limited the application. Results MCF-7/ADR cells have more EMT characteristics than MCF-7 cell. EMT in MCF-7/ADR cells promotes the development of drug resistance via apoptosis resistance and facilitating the expression of P-gp. The anti-cancer effect of DOX enhanced by the decreasing of drug resistance protein P-gp and apoptosis-related proteins after EMT inhibited in MCF-7/ADR cells. E-PLNs increase the cellular uptake of EMO and restore DOX sensitivity in MCF-7/ADR cells by inhibiting EMT. Conclusion E-PLNs inhibit EMT to enhance the sensitivity of breast cancer to DOX. The combination of E-PLNs and DOX can improve the efficacy of DOX in the treatment of breast cancer, which provides a new method to prevent or delay clinical drug resistance.


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