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Updated: Aug 1, 2025
Studying Triple Negative Breast Cancer Using Orthotopic Breast Cancer Model
Published on: March 20, 2020
Therapeutic Potential of Tumor Metabolic Reprogramming in Triple-Negative Breast Cancer
Gyöngyi Munkácsy1,2, Libero Santarpia3, Balázs Győrffy4,5
1National Laboratory for Drug Research and Development, Magyar Tudósok Körútja 2, 1117 Budapest, Hungary.
Abstract:
Triple-negative breast cancer (TNBC) is the most aggressive subtype of breast cancer, with clinical features of high metastatic potential, susceptibility to relapse, and poor prognosis. TNBC lacks the expression of the estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor 2 (HER2). It is characterized by genomic and transcriptional heterogeneity and a tumor microenvironment (TME) with the presence of high levels of stromal tumor-infiltrating lymphocytes (TILs), immunogenicity, and an important immunosuppressive landscape. Recent evidence suggests that metabolic changes in the TME play a key role in molding tumor development by impacting the stromal and immune cell fractions, TME composition, and activation. Hence, a complex inter-talk between metabolic and TME signaling in TNBC exists, highlighting the possibility of uncovering and investigating novel therapeutic targets. A better understanding of the interaction between the TME and tumor cells, and the underlying molecular mechanisms of cell-cell communication signaling, may uncover additional targets for better therapeutic strategies in TNBC treatment. In this review, we aim to discuss the mechanisms in tumor metabolic reprogramming, linking these changes to potential targetable molecular mechanisms to generate new, physical science-inspired clinical translational insights for the cure of TNBC.
Insights
Triple-negative breast cancer (TNBC) is aggressive due to its metastatic potential. Metabolic changes in the tumor microenvironment (TME) offer novel therapeutic targets for TNBC treatment.
Area of Science:
- Oncology
- Cancer Biology
- Metabolic Signaling
Background:
- Triple-negative breast cancer (TNBC) is an aggressive subtype characterized by high metastatic potential and poor prognosis.
- TNBC lacks estrogen receptor (ER), progesterone receptor (PR), and HER2 expression, presenting unique treatment challenges.
- The tumor microenvironment (TME) in TNBC is complex, featuring high stromal tumor-infiltrating lymphocytes (TILs), immunogenicity, and immunosuppression.
Purpose of the Study:
- To review mechanisms of tumor metabolic reprogramming in TNBC.
- To link metabolic changes to targetable molecular mechanisms within the TME.
- To provide physical science-inspired insights for novel TNBC therapeutic strategies.
Main Methods:
- Literature review focusing on metabolic reprogramming in TNBC.
- Analysis of the interplay between tumor cell metabolism and the TME.
- Exploration of cell-cell communication signaling pathways in TNBC.
Main Results:
- Metabolic alterations within the TME significantly influence tumor development, stromal, and immune cell components.
- A complex crosstalk exists between metabolic signaling and the TME in TNBC.
- Understanding these interactions can reveal new therapeutic targets.
Conclusions:
- Metabolic reprogramming is a critical factor in TNBC progression and TME modulation.
- Targeting metabolic pathways and TME interactions presents promising avenues for TNBC treatment.
- Further research into these mechanisms can lead to innovative clinical strategies for TNBC cure.
