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Updated: Jan 22, 2026
Induction and Analysis of Epithelial to Mesenchymal Transition
Published on: August 27, 2013
Reactive oxygen species induce epithelial‑mesenchymal transition, glycolytic switch, and mitochondrial repression
Su Yeon Lee1, Min Kyung Ju1, Hyun Min Jeon1
1Department of Molecular Biology, College of Natural Sciences, Pusan National University, Busan 46241, Republic of Korea.
Abstract:
Reactive oxygen species (ROS) are important cellular second messengers involved in various aspects of cell signaling. ROS are elevated in multiple types of cancer cells, and this elevation is known to be involved in pathological processes of cancer. Although high levels of ROS exert cytotoxic effects on cancer cells, low levels of ROS stimulate cell proliferation and survival by inducing several pro‑survival signaling pathways. In addition, ROS have been shown to induce epithelial‑mesenchymal transition (EMT), which is essential for the initiation of metastasis. However, the precise mechanism of ROS‑induced EMT remains to be elucidated. In the present study, it was indicated that ROS induce EMT by activating Snail expression, which then represses E‑cadherin expression in MCF‑7 cells. It was further indicated that distal‑less homeobox‑2 (Dlx‑2), one of the human Dlx gene family proteins involved in embryonic development, acts as an upstream regulator of ROS‑induced Snail expression. It was also revealed that ROS treatment induces the glycolytic switch, a phenomenon whereby cancer cells primarily rely on glycolysis instead of mitochondrial oxidative phosphorylation for ATP production, even in the presence of oxygen. In addition, ROS inhibited oxidative phosphorylation and caused cytochrome c oxidase inhibition via the Dlx‑2/Snail cascade. These results suggest that ROS induce EMT, the glycolytic switch and mitochondrial repression by activating the Dlx‑2/Snail axis, thereby playing crucial roles in MCF‑7 cancer cell progression.
Insights
Reactive oxygen species (ROS) promote cancer progression by activating the Dlx-2/Snail pathway, inducing epithelial-mesenchymal transition (EMT), and altering cellular metabolism. This mechanism drives cancer cell proliferation and metastasis.
Area of Science:
- Cell Biology
- Cancer Research
- Biochemistry
Background:
- Reactive oxygen species (ROS) are critical signaling molecules in cellular processes.
- Elevated ROS levels are implicated in cancer development and progression.
- ROS can promote cancer cell survival, proliferation, and metastasis, but the underlying mechanisms require further elucidation.
Purpose of the Study:
- To investigate the precise mechanism by which ROS induce epithelial-mesenchymal transition (EMT) in cancer cells.
- To identify the key molecular players involved in ROS-mediated EMT and metabolic reprogramming.
- To elucidate the role of the Dlx-2/Snail axis in ROS-induced cancer progression.
Main Methods:
- MCF-7 cells were treated with ROS-inducing agents.
- Expression levels of Snail, E-cadherin, and Dlx-2 were analyzed.
- Cellular metabolism, including the glycolytic switch and mitochondrial oxidative phosphorylation, was assessed.
- The Dlx-2/Snail signaling cascade was investigated in relation to ROS effects.
Main Results:
- ROS were found to induce EMT in MCF-7 cells by activating Snail expression and repressing E-cadherin.
- Distal-less homeobox-2 (Dlx-2) was identified as an upstream regulator of ROS-induced Snail expression.
- ROS treatment triggered a glycolytic switch and inhibited mitochondrial oxidative phosphorylation via the Dlx-2/Snail pathway.
- Cytochrome c oxidase activity was inhibited through this cascade.
Conclusions:
- ROS activate the Dlx-2/Snail axis to induce EMT, promoting cancer cell progression.
- The Dlx-2/Snail pathway mediates ROS-induced metabolic reprogramming, including the glycolytic switch and mitochondrial repression.
- This study reveals a novel mechanism by which ROS contribute to cancer metastasis and progression in MCF-7 cells.
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