Related Experiment Video

Updated: Jan 11, 2026

Establishing a Silicosis Rat Model via Exposure of Whole-Body to Respirable Silica
05:03

Establishing a Silicosis Rat Model via Exposure of Whole-Body to Respirable Silica

Published on: October 28, 2022

1.6K

ML385 Attenuates Malignant Progression of Silica-induced Lung Adenocarcinoma Cells through the ROS/NRF2-autophagy

Yanhong Cao1, Wubi Zhou2, Junwen Cai3

  • 1School of Medicine, Anhui University of Science and Technology; Department of Medical Laboratory, Huaian Hospital of Huaian City.

Journal of Visualized Experiments : Jove
|November 17, 2025
PubMed

Insights

Silica exposure promotes lung adenocarcinoma by affecting NRF2 and autophagy. The NRF2 inhibitor ML385 reverses these malignant changes, offering a potential therapeutic strategy for silica-related lung cancer.

Area of Science:

  • * Environmental Health
  • * Molecular Biology
  • * Cancer Research

Background:

  • * Silica exposure is linked to lung adenocarcinoma, but the underlying molecular mechanisms are not fully understood.
  • * The nuclear factor erythroid 2-related factor 2 (NRF2) pathway and autophagy are implicated in cancer progression and response to environmental toxins.
  • * Understanding these pathways is crucial for developing targeted therapies against silica-induced lung cancer.

Purpose of the Study:

  • * To establish a repeatable experimental protocol for investigating silica-induced lung adenocarcinoma.
  • * To explore the inhibitory effect of the NRF2 inhibitor ML385 on malignant progression.
  • * To elucidate the role of the ROS/NRF2-autophagy axis in silica-induced lung cancer.

Main Methods:

  • * Establishment of a silicosis mouse model via intranasal silica perfusion.
  • * In vitro studies using RAW264.7 macrophages treated with silica and ML385.
  • * Analysis of pulmonary fibrosis, immune cell infiltration, protein expression (NRF2, CDK1, VDAC1), autophagic flux, ROS levels, and lung adenocarcinoma cell migration, invasion, and apoptosis.

Main Results:

  • * Silica induced pulmonary fibrosis, immune cell infiltration, and upregulated NRF2, CDK1, and VDAC1 in mice.
  • * Silica inhibited macrophage autophagic flux and reduced ROS levels.
  • * ML385 treatment reversed silica-induced changes, inhibiting malignant progression in lung adenocarcinoma cells.

Conclusions:

  • * The established protocol provides a comprehensive approach for studying silica-related lung adenocarcinoma.
  • * The ROS/NRF2-autophagy axis is a key pathway in silica-induced lung cancer progression.
  • * ML385 demonstrates potential as a therapeutic agent targeting NRF2 for silica-induced lung adenocarcinoma.

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