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Updated: Sep 1, 2025

Induction and Analysis of Epithelial to Mesenchymal Transition
Published on: August 27, 2013
The Role of PTEN in Epithelial-Mesenchymal Transition
Olga Fedorova1, Sergey Parfenyev1, Alexandra Daks1
1Institute of Cytology RAS, 194064 St. Petersburg, Russia.
Abstract:
Phosphatase and Tensin Homolog deleted on Chromosome 10 (PTEN) is one of the critical tumor suppressor genes and the main negative regulator of the PI3K pathway. PTEN is frequently found to be inactivated, either partially or fully, in various malignancies. The PI3K/AKT pathway is considered to be one of the main signaling cues that drives the proliferation of cells. Perhaps it is not surprising, then, that this pathway is hyperactivated in highly proliferative tumors. Importantly, the PI3K/AKT pathway also coordinates the epithelial-mesenchymal transition (EMT), which is pivotal for the initiation of metastases and hence is regarded as an attractive target for the treatment of metastatic cancer. It was shown that PTEN suppresses EMT, although the exact mechanism of this effect is still not fully understood. This review is an attempt to systematize the published information on the role of PTEN in the development of malignant tumors, with a main focus on the regulation of the PI3K/AKT pathway in EMT.
Insights
Phosphatase and Tensin Homolog (PTEN) is a key tumor suppressor gene that regulates the PI3K/AKT pathway. This review explores PTEN's role in cancer, focusing on how it suppresses epithelial-mesenchymal transition (EMT) and metastasis.
Area of Science:
- Oncology
- Molecular Biology
- Cell Biology
Background:
- Phosphatase and Tensin Homolog (PTEN) is a critical tumor suppressor gene.
- PTEN acts as the primary negative regulator of the phosphoinositide 3-kinase (PI3K) pathway.
- Inactivation of PTEN is common in many cancers, leading to pathway hyperactivation.
Purpose of the Study:
- To review the role of PTEN in malignant tumor development.
- To focus on PTEN's regulation of the PI3K/AKT pathway in epithelial-mesenchymal transition (EMT).
- To systematize current knowledge on PTEN's tumor suppressive functions.
Main Methods:
- Literature review and synthesis of published research.
- Analysis of PTEN's involvement in cancer signaling pathways.
- Focus on PTEN's impact on EMT regulation.
Main Results:
- PTEN inactivation is linked to hyperactivation of the PI3K/AKT pathway.
- The PI3K/AKT pathway drives cell proliferation and is crucial in tumor growth.
- PTEN suppresses EMT, a process vital for cancer metastasis, though mechanisms require further elucidation.
Conclusions:
- PTEN plays a significant role in suppressing tumor development and metastasis.
- Understanding PTEN's regulation of EMT is crucial for developing targeted cancer therapies.
- Further research into PTEN's precise mechanisms in EMT is warranted.
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