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Updated: Oct 10, 2025

Studying Triple Negative Breast Cancer Using Orthotopic Breast Cancer Model
Published on: March 20, 2020
Regulation of the tumor suppressor PTEN in triple-negative breast cancer
Chengsen Chai1, H Helena Wu2, Yasser Abuetabh2
1370 Heritage Medical Research Center, Department of Laboratory Medicine and Pathology, University of Alberta, Edmonton, Alberta T6G 2S2, Canada; Key Laboratory of Clinical Laboratory Diagnostics, College of Laboratory Medicine, Chongqing Medical University, Chongqing, 400016, China.
Abstract:
Triple-negative breast cancer (TNBC) is a subtype of breast cancer (BCa) in which estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor 2 (HER-2) are not expressed. Although TNBC cases account for approximately 15% of all BCa cases, TNBC patients' prognosis is poor compared with that of other BCa subtypes. Phosphatase and tensin homolog deleted on chromosome 10 (PTEN) plays an important role in cell proliferation and migration by negatively regulating the PI3K/Akt pathway. PTEN is one of the most commonly inactivated tumor suppressors in BCa. PTEN inactivity is associated with larger tumor sizes, multiple lymph node metastases, and an aggressive triple-negative phenotype. This review primarily focuses on two key points: (1) PTEN and its function. (2) The regulation of tumor suppressor PTEN in TNBC. We provide a summary of genomic alterations of PTEN in BCa. We further discuss the transcriptional regulation of PTEN and how PTEN is regulated by posttranscription and posttranslational modification, as well as by protein interactions. Finally, we discuss the perspectives of the PTEN protein in TNBC.
Insights
Triple-negative breast cancer (TNBC) has a poor prognosis. This review explores how the tumor suppressor PTEN, crucial for cell regulation, is altered and functions in TNBC.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Triple-negative breast cancer (TNBC) lacks ER, PR, and HER-2 expression, leading to poorer patient outcomes.
- Phosphatase and tensin homolog deleted on chromosome 10 (PTEN) is a key tumor suppressor regulating the PI3K/Akt pathway.
- PTEN inactivation correlates with aggressive TNBC features like larger tumors and lymph node metastasis.
Purpose of the Study:
- To review the function of PTEN in cancer biology.
- To summarize PTEN's genomic alterations in breast cancer.
- To elucidate the regulatory mechanisms of PTEN in TNBC.
Main Methods:
- Literature review focusing on PTEN's role and regulation in TNBC.
- Summary of genomic alterations affecting PTEN in breast cancer.
- Discussion of transcriptional, post-transcriptional, and post-translational regulation of PTEN.
Main Results:
- PTEN is frequently inactivated in breast cancer, particularly in TNBC.
- PTEN's tumor-suppressive functions are critical in controlling cell proliferation and migration.
- PTEN is subject to complex regulation including genomic alterations, transcriptional control, and post-translational modifications.
Conclusions:
- Understanding PTEN's multifaceted regulation in TNBC is crucial for developing targeted therapies.
- PTEN represents a significant therapeutic target for improving outcomes in triple-negative breast cancer.
- Further research into PTEN's regulatory network may unlock novel treatment strategies for TNBC.
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