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Updated: May 31, 2026
11:42
Induction of Mesenchymal-Epithelial Transitions in Sarcoma Cells
Published on: April 7, 2017
Epithelial-mesenchymal transition induced by senescent fibroblasts
Remi-Martin Laberge1, Pierre Awad, Judith Campisi
1Buck Institute for Research on Aging, 8001 Redwood Boulevard, Novato, CA, 94945, USA.
Summary
Cellular senescence, a tumor-suppressive mechanism, can paradoxically promote cancer metastasis. Senescence-associated secretory phenotype (SASP) factors can induce epithelial-mesenchymal transitions (EMTs), driving tumor progression.
Area of Science:
- Cell Biology
- Cancer Biology
- Aging Research
Background:
- Epithelial-mesenchymal transitions (EMTs) are dynamic cellular processes crucial for development and wound healing, but also implicated in cancer metastasis.
- Cellular senescence, a state of permanent cell cycle arrest, acts as a tumor suppressor.
- Senescent cells can acquire a senescence-associated secretory phenotype (SASP), influencing the tissue microenvironment.
Purpose of the Study:
- To summarize the impact of SASP factors on tissue microenvironments.
- To elucidate how SASP factors stimulate tumor progression via EMT induction.
Main Methods:
- Review of existing literature on EMT, senescence, and SASP.
- Analysis of the role of specific SASP factors, such as interleukins.
Main Results:
- SASP factors can alter the tissue microenvironment, promoting inflammation.
- SASP can induce EMT in nearby epithelial cells, facilitating tumor invasion and metastasis.
- Interleukins are key SASP components that drive pro-tumorigenic effects.
Conclusions:
- While senescence is tumor-suppressive, its SASP can paradoxically promote cancer progression.
- SASP-induced EMT is a significant mechanism of tumor metastasis.
- Targeting SASP factors may offer therapeutic strategies against cancer metastasis.
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