Thermo and pH dual-controlled charge reversal amphiphilic graft copolymer micelles for overcoming drug resistance in cancer cells

2015 ◽  
Vol 3 (22) ◽  
pp. 4585-4596 ◽  
Author(s):  
Haitao Zhang ◽  
Xiaodong Fan ◽  
Fei Li ◽  
Rongtian Suo ◽  
Hui Li ◽  
...  
Keyword(s):  
Drug Resistance ◽  
Cancer Cells ◽  
Cellular Uptake ◽  
Graft Copolymer ◽  
Multi Drug Resistance ◽  
Charge Reversal ◽  
Amphiphilic Graft Copolymer ◽  
Copolymer Micelle ◽  
Copolymer Micelles

A novel thermo and pH dual-controlled charge reversal PSMA89-g-P(DMA16-co-SD56) graft copolymer micelle was developed with effectively enhanced cellular uptake for overcoming multi-drug resistance in cancer cells.

Strategies to Overcome Multi-Drug Resistance in Cancer Cells: the Contribution of siRNA and Nanotechnologies

2016 ◽  
Vol 20 (28) ◽  
pp. 2971-2982
Author(s):  
Cristina Mambet ◽  
Mihaela Chivu-Economescu ◽  
Lilia Matei ◽  
Mihai Stoian ◽  
Coralia Bleotu
Keyword(s):  
Drug Resistance ◽  
Cancer Cells ◽  
Multi Drug Resistance

PEAK1 promotes invasion and metastasis and confers drug resistance in breast cancer

2021 ◽  
Author(s):  
xingang wang ◽  
YAN ZHENG ◽  
YU WANG
Keyword(s):  
Breast Cancer ◽  
Drug Resistance ◽  
Cell Growth ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Multi Drug Resistance ◽  
Cancer Tissues

Abstract Background and AimsPseudopodium-enriched atypical kinase 1 (PEAK1) has reported to be upregulated in human malignancies and related with poor prognosis. Enhanced PEAK1 expression facilitates tumor cell survival, invasion, metastasis and chemoresistance. However, the role of PEAK1 in breast cancer is not clear. Here, we investigated the PEAK1 expression in breast cancer and analyzed its relation with clinicopathological status and chemotherapy resistance to the neoadjuvant chemotherapy (NAC). We also investigated the role of PEAK1 on breast cancer cells in vitro and in vivo. MethodsImmunohistochemistry (IHC) was performed in 112 surgical resected breast cancer tissues. The associations between clinicopathological status, multi-drug resistance and PEAK1 expression were determined. Effect of PEAK1 overexpression or down-expression on proliferation, colony formation, invasion, migration, metastasis and Doxorubicin sensitivity in the MCF-7 cells in vitro and in vivo was detected. ResultsPEAK1 was overexpressed in breast cancer tissues and NAC -resistant breast cancer tissues. High PEAK1 expression was related with tumor size, high tumor grade, T stage, LN metastasis, recurrence, Ki-67 expression, Her-2 expression and multi-drug resistance. Targeting PEAK1 inhibited cell growth, invasion, metastasis and reversed chemoresistance to Doxorubicin in breast cancer cells in vitro and in vivo. ConclusionHigh PEAK1 expression was associated with invasion, metastasis and chemoresistance of breast cancers. Furthermore, targeting PEAK1 could inhibit cell growth and metastasis, and reverse chemoresistance in breast cancer cells, which provides an effective treatment strategies for breast cancer.

scholarly journals Berberine Improves Chemo-Sensitivity to Cisplatin by Enhancing Cell Apoptosis and Repressing PI3K/AKT/mTOR Signaling Pathway in Gastric Cancer

2020 ◽  
Vol 11 ◽  
Author(s):  
Yingying Kou ◽  
Bending Tong ◽  
Weiqing Wu ◽  
Xiangqing Liao ◽  
Min Zhao
Keyword(s):  
Gastric Cancer ◽  
Drug Resistance ◽  
Multidrug Resistance ◽  
Cell Viability ◽  
Cancer Cells ◽  
Cell Apoptosis ◽  
Mtor Signaling ◽  
Multi Drug Resistance ◽  
Gastric Cancer Cells

Gastric cancer is one of the most common malignancies ranks as the second leading cause of cancer-related mortality in the world. Cisplatin (DDP) is commonly used for gastric cancer treatment, whereas recurrence and metastasis are common because of intrinsic and acquired DDP-resistance. The aim of this study is to examine the effects of berberine on the DDP-resistance in gastric cancer and explore the underling mechanisms. In this study, we established the DDP-resistant gastric cancer cells, where the IC50 values of DDP in the BGC-823/DDP and SGC-7901/DDP were significantly higher than that in the corresponding parental cells. Berberine could concentration-dependently inhibited the cell viability of BGC-823 and SGC-7901 cells; while the inhibitory effects of berberine on the cell viability were largely attenuated in the DDP-resistant cells. Berberine pre-treatment significantly sensitized BGC-823/DDP and SGC-7901/DDP cells to DDP. Furthermore, berberine treatment concentration-dependently down-regulated the multidrug resistance-associated protein 1 and multi-drug resistance-1 protein levels in the BGC-823/DDP and SGC7901/DDP cells. Interestingly, the cell apoptosis of BGC-823/DDP and SGC-7901/DDP cells was significantly enhanced by co-treatment with berberine and DDP. The results from animals also showed that berberine treatment sensitized SGC-7901/DDP cells to DDP in vivo. Mechanistically, berberine significantly suppressed the PI3K/AKT/mTOR in the BGC-823/DDP and SGC-7901/DDP cells treated with DDP. In conclusion, we observed that berberine sensitizes gastric cancer cells to DDP. Further mechanistic findings suggested that berberine-mediated DDP-sensitivity may be associated with reduced expression of drug transporters (multi-drug resistance-1 and multidrug resistance-associated protein 1), enhanced apoptosis and repressed PI3K/AKT/mTOR signaling.

The enriched fraction of Vernonia cinerea L. induces apoptosis and inhibits multi-drug resistance transporters in human epithelial cancer cells

2014 ◽  
Vol 158 ◽  
pp. 33-42 ◽  
Author(s):  
Asmy Appadath Beeran ◽  
Naseer Maliyakkal ◽  
Chamallamudi Mallikarjuna Rao ◽  
Nayanabhirama Udupa
Keyword(s):  
Drug Resistance ◽  
Cancer Cells ◽  
Multi Drug Resistance ◽  
Epithelial Cancer ◽  
Vernonia Cinerea

scholarly journals Acidosis induces multi-drug resistance in rat prostate cancer cells (AT1)in vitroandin vivoby increasing the activity of the p-glycoproteinviaactivation of p38

2008 ◽  
Vol 123 (11) ◽  
pp. 2532-2542 ◽  
Author(s):  
Christoph Sauvant ◽  
Martin Nowak ◽  
Claudia Wirth ◽  
Bettina Schneider ◽  
Anne Riemann ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Drug Resistance ◽  
Cancer Cells ◽  
Multi Drug Resistance ◽  
Prostate Cancer Cells ◽  
Rat Prostate
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