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Related Experiment Video

Updated: Jun 6, 2026

The Establishment of a Lung Colonization Assay for Circulating Tumor Cell Visualization in Lung Tissues
07:39

The Establishment of a Lung Colonization Assay for Circulating Tumor Cell Visualization in Lung Tissues

Published on: June 16, 2018

Methotrexate binding causes structural and functional changes in lung cystatin.

Mohd Shahnawaz Khan1, Medha Priyadarshini, Sadia Sumbul

  • 1Department of Biochemistry, Aligarh Muslim University, U.P., India.

Acta Biochimica Polonica
|December 3, 2010
PubMed
Summary

The antineoplastic drug methotrexate (MTX) binds to and inactivates lung cystatin, a cysteine protease inhibitor. This interaction, driven by hydrogen bonds and hydrophobic forces, may explain off-target tissue damage from MTX treatment.

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Last Updated: Jun 6, 2026

The Establishment of a Lung Colonization Assay for Circulating Tumor Cell Visualization in Lung Tissues
07:39

The Establishment of a Lung Colonization Assay for Circulating Tumor Cell Visualization in Lung Tissues

Published on: June 16, 2018

Area of Science:

  • Biochemistry
  • Pharmacology
  • Molecular Biology

Background:

  • Cysteine proteinase and inhibitor regulation is crucial for lung diseases like cancer and fibrosis.
  • An imbalance between proteases and antiproteases exacerbates disease progression.

Purpose of the Study:

  • To investigate the impact of methotrexate (MTX) on the functional and structural integrity of lung cystatin.
  • To explore the binding interactions between MTX and goat lung cystatin (GLC-I).

Main Methods:

  • UV-absorption, FT-IR, and fluorescence spectroscopy were employed to study MTX-GLC-I binding.
  • Fluorescence quenching and Stern-Volmer analysis were used to confirm binding and mechanism.
  • Thermodynamic parameters (ΔH⁰, ΔS⁰) were calculated to elucidate interaction forces.

Main Results:

  • Methotrexate (MTX) binding to goat lung cystatin (GLC-I) was confirmed by fluorescence quenching.
  • Hydrogen bonds and hydrophobic interactions were identified as key binding forces.
  • MTX (7 µM) led to complete inactivation of lung cystatin within 6 hours, with FT-IR indicating structural changes.

Conclusions:

  • Methotrexate binds to and inactivates lung cystatin, suggesting a mechanism for off-target effects.
  • Understanding this interaction could aid in designing strategies to mitigate MTX-induced tissue injury.