scholarly journals CD44 promotes multi-drug resistance by protecting P-glycoprotein from FBXO21-mediated ubiquitination

Oncotarget ◽  
2015 ◽  
Vol 6 (28) ◽  
pp. 26308-26321 ◽  
Author(s):  
Abhilash K. Ravindranath ◽  
Swayamjot Kaur ◽  
Roman P. Wernyj ◽  
Muthu N. Kumaran ◽  
Karl E. Miletti-Gonzalez ◽  
...  
Keyword(s):  
Drug Resistance ◽  
Multi Drug Resistance ◽  
P Glycoprotein

Synthesis and Biological Evaluation of C-Aromataxane Derivatives as P-Glycoprotein-Mediated Multi Drug Resistance Reversal Agents

Heterocycles ◽  
2015 ◽  
Vol 90 (1) ◽  
pp. 482
Author(s):  
Takayuki Doi ◽  
Naoko Yamaguchi ◽  
Kosuke Ohsawa ◽  
Kazuoki Nakai ◽  
Masahito Yoshida ◽  
...  
Keyword(s):  
Drug Resistance ◽  
Biological Evaluation ◽  
Multi Drug Resistance ◽  
Reversal Agents ◽  
P Glycoprotein ◽  
Resistance Reversal ◽  
Synthesis And Biological Evaluation

scholarly journals Cancer drug pan-resistance: pumps, cancer stem cells, quiescence, epithelial to mesenchymal transition, blocked cell death pathways, persisters or what?

Open Biology ◽  
2012 ◽  
Vol 2 (5) ◽  
pp. 120066 ◽  
Author(s):  
Piet Borst
Keyword(s):  
Stem Cells ◽  
Drug Resistance ◽  
Epithelial To Mesenchymal Transition ◽  
Residual Disease ◽  
Cancer Drug ◽  
Multi Drug Resistance ◽  
Mesenchymal Transition ◽  
Cell Death Pathways ◽  
P Glycoprotein ◽  
Mouse Tumour

Although chemotherapy of tumours has scored successes, drug resistance remains the major cause of death of cancer patients. Initial treatment often leaves residual disease, from which the tumour regrows. Eventually, most tumours become resistant to all available chemotherapy. I call this pan-resistance to distinguish it from multi-drug resistance, usually describing resistance caused by upregulation of drug transporters, such as P-glycoprotein. In this review, I discuss mechanisms proposed to explain both residual disease and pan-resistance. Although plausible explanations are at hand for residual disease, pan-resistance is still a mystery. My conclusion is that it is time for a major effort to solve this mystery using the new genetically modified mouse tumour models that produce real tumours resembling cancer in human patients.

99Tcm-sestamibi as an agent for imaging P-glycoprotein-mediated multi-drug resistance

1995 ◽  
Vol 16 (4) ◽  
pp. 253-257 ◽  
Author(s):  
J. R. BALLINGER ◽  
H. A. HUA ◽  
B. W. BERRY ◽  
P. FIRBY ◽  
I. BOXEN
Keyword(s):  
Drug Resistance ◽  
Multi Drug Resistance ◽  
P Glycoprotein

scholarly journals The Establishment of Quantitatively Regulating Expression Cassette with sgRNA Targeting BIRC5 to Elucidate the Synergistic Pathway of Survivin with P-Glycoprotein in Cancer Multi-Drug Resistance

2022 ◽  
Vol 9 ◽  
Author(s):  
Changping Deng ◽  
Fabiao Hu ◽  
Zhangting Zhao ◽  
Yiwen Zhou ◽  
Yuping Liu ◽  
...  
Keyword(s):  
Drug Resistance ◽  
Survivin Expression ◽  
Regulatory System ◽  
Multi Drug Resistance ◽  
Specific Gene ◽  
Expression Levels ◽  
P Glycoprotein ◽  
Biological Phenomena ◽  
Reversal Index ◽  
Mcf 7

Quantitative analysis and regulating gene expression in cancer cells is an innovative method to study key genes in tumors, which conduces to analyze the biological function of the specific gene. In this study, we found the expression levels of Survivin protein (BIRC5) and P-glycoprotein (MDR1) in MCF-7/doxorubicin (DOX) cells (drug-resistant cells) were significantly higher than MCF-7 cells (wild-type cells). In order to explore the specific functions of BIRC5 gene in multi-drug resistance (MDR), a CRISPR/Cas9-mediated knocking-in tetracycline (Tet)-off regulatory system cell line was established, which enabled us to regulate the expression levels of Survivin quantitatively (clone 8 named MCF-7/Survivin was selected for further studies). Subsequently, the determination results of doxycycline-induced DOX efflux in MCF-7/Survivin cells implied that Survivin expression level was opposite to DOX accumulation in the cells. For example, when Survivin expression was down-regulated, DOX accumulation inside the MCF-7/Survivin cells was up-regulated, inducing strong apoptosis of cells (reversal index 118.07) by weakening the release of intracellular drug from MCF-7/Survivin cells. Also, down-regulation of Survivin resulted in reduced phosphorylation of PI3K, Akt, and mTOR in MCF-7/Survivin cells and significantly decreased P-gp expression. Previous studies had shown that PI3K/Akt/mTOR could regulate P-gp expression. Therefore, we speculated that Survivin might affect the expression of P-gp through PI3K/Akt/mTOR pathway. In summary, this quantitative method is not only valuable for studying the gene itself, but also can better analyze the biological phenomena related to it.

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