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Published on: June 9, 2023
Expression of mTOR Signaling Pathway Molecules in Triple-Negative Breast Cancer
Kei Ito1,2, Hideaki Ogata3, Naoko Honma4
1Department of Pathology, Toho University Graduate School of Medicine, Tokyo, Japan, k-ito@tius.ac.jp.
Introduction:
Triple-negative breast cancer (TNBC), which lacks expression of estrogen receptor (ER), progesterone receptor (PgR), and epidermal growth factor receptor 2 (HER2), currently has no effective hormonal or molecular target therapy.
Objective And Methods:
To elucidate the role of the mammalian target of rapamycin (mTOR) signaling pathway in TNBC, the expression of molecules involved in mTOR signaling including mTOR, phosphorylated (p)-mTOR, p-4EBP1, GLUT1, GLUT3, HIF-1α, and Ki67 was investigated by immunohistochemistry in 35 TNBC and 81 non-TNBC cases.
Results:
Expression of p-mTOR, the activated form of mTOR, but not unphosphorylated mTOR, was significantly higher in non-TNBC cases than in TNBC cases. Expression of p-4EBP1, GLUT1, and GLUT3 was higher in TNBC cases than in non-TNBC cases. When the localization of p-mTOR was classified as nuclear, perinuclear, or cytoplasmic, nuclear localization of p-mTOR was observed more frequently in TNBC than in non-TNBC cases and was correlated with the expression of GLUT1 and GLUT3, which was related to proliferation activity examined with Ki67.
Conclusions:
mTOR signaling regulates cell proliferation in some cases of TNBC and may be a potential target of molecular therapy for TNBC.
Insights
Mammalian target of rapamycin (mTOR) signaling is altered in triple-negative breast cancer (TNBC). Nuclear mTOR activation correlates with proliferation markers, suggesting mTOR as a potential therapeutic target for TNBC.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- Triple-negative breast cancer (TNBC) lacks targeted therapy options due to absent ER, PgR, and HER2 expression.
- Investigating signaling pathways is crucial for identifying new therapeutic strategies for TNBC.
Purpose of the Study:
- To explore the role of the mammalian target of rapamycin (mTOR) signaling pathway in TNBC.
- To analyze the expression of key mTOR pathway molecules in TNBC versus non-TNBC.
Main Methods:
- Immunohistochemistry was used to assess the expression of mTOR, p-mTOR, p-4EBP1, GLUT1, GLUT3, HIF-1α, and Ki67.
- The study included 35 TNBC and 81 non-TNBC cases.
Main Results:
- Activated mTOR (p-mTOR) was less frequent in TNBC compared to non-TNBC.
- TNBC showed higher expression of p-4EBP1, GLUT1, and GLUT3.
- Nuclear p-mTOR in TNBC correlated with GLUT1, GLUT3, and proliferation marker Ki67.
Conclusions:
- mTOR signaling influences cell proliferation in a subset of TNBC cases.
- The mTOR pathway represents a potential molecular target for TNBC treatment.
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