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Quantifiable and Inexpensive Cell-Free Fluorescent Method to Confirm the Ability of Novel Compounds to Chelate Iron
05:36

Quantifiable and Inexpensive Cell-Free Fluorescent Method to Confirm the Ability of Novel Compounds to Chelate Iron

Published on: February 23, 2024

Targeting mitochondrial cell death pathway to overcome drug resistance with a newly developed iron chelate

Avishek Ganguly1, Soumya Basu, Paramita Chakraborty

  • 1Department of In Vitro Carcinogenesis and Cellular Chemotherapy, Chittaranjan National Cancer Institute, Kolkata, India.

Plos One
|June 29, 2010
PubMed
Abstract

Insights

A novel iron complex, FeNG, effectively kills both drug-sensitive and drug-resistant T lymphoblastic leukemia cells. This new compound overcomes multi-drug resistance (MDR) by inducing apoptosis through a reactive oxygen species-mediated mitochondrial pathway.

Area of Science:

  • Biochemistry
  • Cancer Biology
  • Medicinal Chemistry

Background:

  • Multi-drug resistance (MDR) is a significant challenge in cancer chemotherapy.
  • P-glycoprotein (P-gp) is a key factor in MDR, limiting treatment efficacy.
  • Novel compounds not substrates of P-gp are needed to combat resistant cancers.

Purpose of the Study:

  • To synthesize and evaluate a novel redox-active iron complex, FeNG, for its efficacy against drug-resistant cancer cells.
  • To investigate the mechanism of action of FeNG in overcoming MDR.

Main Methods:

  • Synthesis of a novel Fe(II) complex, iron N-(2-hydroxy acetophenone) glycinate (FeNG).
  • Evaluation of FeNG's cytotoxic effects on doxorubicin-resistant and sensitive T lymphoblastic leukemia cells.
  • Assessment of FeNG's mechanism of action, including apoptosis induction and reactive oxygen species (ROS) generation, with N-acetyl-cysteine (NAC) as a control.

Main Results:

  • FeNG demonstrated potent cytotoxicity against both drug-sensitive and drug-resistant T lymphoblastic leukemia cells, irrespective of their MDR phenotype.
  • FeNG induced apoptosis in doxorubicin-resistant cells via the mitochondrial pathway, involving the generation of ROS.
  • The antioxidant NAC successfully blocked FeNG-induced ROS generation and abrogated apoptosis, confirming the role of ROS in FeNG's mechanism.

Conclusions:

  • FeNG is a novel, redox-active metal chelate with significant potential as a therapeutic agent.
  • FeNG effectively overcomes multi-drug resistance in T lymphoblastic leukemia by inducing apoptosis.
  • This study highlights FeNG as a promising candidate for treating drug-resistant cancers.

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