原创力文档targeting mitochondrial cell death pathway to overcome drug resistance with a newly developed iron chelate针对线粒体细胞死亡途径克服耐药性新开发的铁螯合物.pdfVIP
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targeting mitochondrial cell death pathway to overcome drug resistance with a newly developed iron chelate针对线粒体细胞死亡途径克服耐药性新开发的铁螯合物
Targeting Mitochondrial Cell Death Pathway to
Overcome Drug Resistance with a Newly Developed Iron
Chelate
1 1 1 1 2
Avishek Ganguly , Soumya Basu , Paramita Chakraborty , Shilpak Chatterjee , Avijit Sarkar ,
2 1
Mitali Chatterjee , Soumitra Kumar Choudhuri *
1 Department of In Vitro Carcinogenesis and Cellular Chemotherapy, Chittaranjan National Cancer Institute, Kolkata, India, 2 Department of Pharmacology, Institute of
Post Graduate Medical Education and Research, Kolkata, India
Abstract
Background: Multi drug resistance (MDR) or cross-resistance to multiple classes of chemotherapeutic agents is a major
obstacle to successful application of chemotherapy and a basic problem in cancer biology. The multidrug resistance gene,
MDR1, and its gene product P-glycoprotein (P-gp) are an important determinant of MDR. Therefore, there is an urgent need
for development of novel compounds that are not substrates of P-glycoprotein and are effective against drug-resistant
cancer.
Methodology/Principal Findings: In this present study, we have synthesized a novel, redox active Fe (II) complex (chelate),
iron N- (2-hydroxy acetophenone) glycinate (FeNG). The structure of the complex has been determined by spectroscopic
means. To evaluate the cytotoxic effect of FeNG we used doxorubicin resistant and/or sensitive T lymphoblastic leukemia
cells and show that FeNG kills both the cell types irrespective of their MDR phenotype. Moreover, FeNG induces apoptosis in
doxorubicin resistance T lymphoblastic leukemia cell through mitochondrial pathway via generation reactive oxygen
species (ROS). This is substantiated by the fact that the antioxi
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