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Updated: May 20, 2026

Induction and Analysis of Epithelial to Mesenchymal Transition
Published on: August 27, 2013
Inflammation linking EMT and cancer stem cells
Chenchen Zhou1, Jeffrey Liu, Yaling Tang
1State Key Laboratory of Oral Diseases, West China Hospital of Stomatology, Sichuan University, No 14, Sec 3, Renminnan Road, Chengdu Sichuan 610041, People's Republic of China.
Cancer cells rapidly change during metastasis, including epithelial-mesenchymal transition (EMT) and acquiring cancer stem cells (CSCs) properties. This review explores these changes in an inflammation microenvironment to understand and prevent tumor invasion and metastasis.
Area of Science:
- Oncology
- Cell Biology
- Cancer Research
Background:
- Tumor metastasis involves dynamic cancer cell state transitions, such as epithelial-mesenchymal transition (EMT) and acquisition of cancer stem cells (CSCs) properties.
- The tumor microenvironment, particularly inflammation, significantly influences cancer cell plasticity and promotes tumor progression.
- Understanding these cellular changes is crucial for developing effective anti-cancer strategies.
Purpose of the Study:
- To review the dynamic changes cancer cells undergo during metastasis, focusing on the EMT to CSCs transition.
- To elucidate the role of the inflammatory microenvironment in promoting these cellular transformations.
- To provide insights into the mechanisms of invasion and metastasis for developing prevention strategies.
Main Methods:
- Literature review of studies on cancer cell plasticity during metastasis.
- Analysis of the interplay between cancer cell states (EMT, CSCs) and the tumor microenvironment.
- Synthesis of current knowledge on inflammation-driven tumor promotion and metastasis.
Main Results:
- Cancer cells exhibit remarkable adaptability, transitioning between EMT, CSCs, and MET states to survive and spread.
- Inflammation acts as a potent promoter, creating a microenvironment conducive to sustained cancer cell plasticity and metastasis.
- These dynamic changes are key to overcoming anti-tumorigenic pressures and establishing secondary tumors.
Conclusions:
- The plasticity of cancer cells, particularly the EMT-CSC axis within an inflammatory milieu, is central to tumor invasion and metastasis.
- Targeting these cellular transitions and the inflammatory microenvironment holds promise for preventing cancer metastasis.
- Further research into these mechanisms can guide the development of novel therapeutic interventions.
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