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Related Experiment Video

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In Vitro Scratch Assay to Demonstrate Effects of Arsenic on Skin Cell Migration

In Vitro Scratch Assay to Demonstrate Effects of Arsenic on Skin Cell Migration

Published on: February 23, 2019

Molecular changes during arsenic-induced cell transformation.

Guanwu Li¹, Lai-Sheung Lee, Muyao Li

¹Department of Biochemistry/Open Laboratory for Tumor Molecular Biology, Shantou University Medical College, Shantou, China.

Journal of Cellular Physiology

|February 24, 2011

Summary

Arsenite exposure causes cell transformation and proliferation through oxidative stress and the Ras/Erk pathway. Antioxidants can inhibit these effects, highlighting the role of reactive oxygen species (ROS) in arsenite-induced lung cell changes.

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Area of Science:

Environmental Health
Toxicology
Molecular Biology

Background:

Arsenic compounds are widespread environmental metalloids linked to various cancers.
The precise molecular mechanisms of arsenic-induced carcinogenesis are not fully understood.
Oxidative stress is a proposed mechanism in arsenic toxicity.

Purpose of the Study:

To investigate the role of oxidative stress in arsenite-induced cell transformation.
To elucidate the involvement of the reactive oxygen species (ROS)-mediated Ras/Erk pathway in arsenite toxicity.
To characterize the effects of arsenite on rat lung epithelial cells (LECs).

Main Methods:

Induction of rat lung epithelial cell (LEC) transformation and epithelial-mesenchymal transition by arsenite.
Assessment of the Ras/Erk and phosphoinositide 3-kinase/protein kinase B signaling pathways.
Evaluation of cell proliferation and the impact of antioxidant treatment.

Main Results:

Arsenite induced LEC transformation, epithelial-mesenchymal transition, and cell proliferation.
The extracellular signal-regulated kinase (Erk) pathway was activated, but the phosphoinositide 3-kinase/protein kinase B pathway was not.
Concurrent treatment with antioxidants inhibited arsenite-induced cell transformation and p-ERK induction, indicating ROS mediation.

Conclusions:

Arsenite-induced cell transformation and proliferation in LECs are mediated by oxidative stress via the ROS-dependent Ras/Erk pathway.
Antioxidants effectively inhibit arsenite-induced cellular changes, underscoring the critical role of ROS.
These findings contribute to understanding the molecular mechanisms of arsenic carcinogenesis.