Epithelial-mesenchymal transition (EMT)

Definition

Epithelial-mesenchymal transition (EMT) is a biological process where epithelial cells lose their cell polarity and adhesion properties to acquire migratory and invasive characteristics typical of mesenchymal cells. This process plays a critical role in various physiological events, such as embryogenesis, wound healing, and importantly, in cancer metastasis, enabling cancer cells to invade surrounding tissues and spread to distant sites in the body.

5 Must Know Facts For Your Next Test

1. EMT is a key mechanism that allows carcinoma cells to detach from the primary tumor and invade the surrounding stroma, contributing to tumor progression.
2. Key transcription factors like Snail, Twist, and Zeb are often upregulated during EMT, promoting the downregulation of epithelial markers and the upregulation of mesenchymal markers.
3. The reversal of EMT is referred to as mesenchymal-epithelial transition (MET), which is also critical in metastatic colonization and secondary tumor formation.
4. Understanding EMT can lead to potential therapeutic strategies aimed at preventing cancer metastasis by targeting the signaling pathways involved in this transition.
5. Cancer stem cells often exhibit features of EMT, making it an important area of research for understanding tumor heterogeneity and treatment resistance.

Review Questions

• How does epithelial-mesenchymal transition (EMT) contribute to cancer metastasis?
  • EMT contributes to cancer metastasis by allowing epithelial cancer cells to lose their adhesion properties and gain migratory capabilities. This transition enables the cells to invade surrounding tissues, enter the bloodstream, and establish secondary tumors at distant sites. The acquisition of mesenchymal characteristics enhances the invasive potential of these cells, making them more capable of spreading throughout the body.
• Discuss the role of transcription factors in regulating epithelial-mesenchymal transition (EMT) in cancer cells.
  • Transcription factors such as Snail, Twist, and Zeb play pivotal roles in regulating EMT by activating genes associated with mesenchymal characteristics while repressing genes linked to epithelial traits. These factors orchestrate the molecular changes necessary for cell detachment and migration. Their expression is often triggered by various signaling pathways activated by growth factors in the tumor microenvironment, facilitating the cancer cells' transition into a more invasive state.
• Evaluate the potential therapeutic implications of targeting epithelial-mesenchymal transition (EMT) in cancer treatment strategies.
  • Targeting EMT presents a promising therapeutic approach in cancer treatment as it could help prevent or reduce metastasis. By inhibiting key signaling pathways or transcription factors involved in the EMT process, it may be possible to maintain the epithelial characteristics of cancer cells and diminish their invasive potential. Furthermore, understanding how EMT contributes to tumor heterogeneity could lead to more effective treatments that address not only the primary tumor but also metastatic disease, ultimately improving patient outcomes.

Related terms

Metastasis: The process by which cancer cells spread from the primary tumor to distant organs or tissues, often facilitated by EMT.

Cadherins: A class of cell adhesion molecules that play a crucial role in maintaining the integrity of epithelial tissue; their downregulation is a hallmark of EMT.

Growth Factors: Proteins that stimulate cell proliferation and differentiation, often involved in signaling pathways that induce EMT during cancer progression.