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Updated: Sep 14, 2025
Isolation and Functional Assessment of Human Breast Cancer Stem Cells from Cell and Tissue Samples
Published on: October 2, 2020
Translational drugs targeting cancer stem cells in triple-negative breast cancer
Felipe P de Oliveira1, Mateus L Nogueira1, Alexandre F C Galvão1
1Gonçalo Moniz Institute, Oswaldo Cruz Foundation (IGM-FIOCRUZ/BA), Salvador, Bahia 40296-710, Brazil.
Abstract:
Triple-negative breast cancer (TNBC) is defined by the lack of expression of estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor 2 (HER2). It is unresponsive to targeted therapy and is associated with a high degree of malignancy, a high propensity for metastasis, high recurrence rates, and poor prognosis. In the modern concept of cancer biology, a subset of cancer cells known as tumor-initiating cells or cancer stem cells (CSCs) are defined as essential for the development and dissemination of cancer. These are a population of highly tumorigenic and self-renewing pluripotent cells that are inherently associated to the initiation, dissemination, relapse, and development of drug resistance. Specifically, some cell signaling pathways may affect the ability of CSCs to self-renew, differentiate, proliferate, and survive. To guide future research, in this review, we address compounds that target cell signaling and eliminate TNBC stem cells. Potential translational inhibitors of the Hedgehog, nuclear factor κB (NF-κB), Wnt, Notch, Hippo, TGF-β, JAK/STAT, and PI3K/AKT/mTOR cell signaling pathways are discussed, with a focus on TNBC stem cell eradication.
Insights
Triple-negative breast cancer (TNBC) is aggressive and hard to treat. This review explores targeting cancer stem cells (CSCs) by inhibiting key cell signaling pathways to improve TNBC treatment outcomes.
Area of Science:
- Oncology
- Cancer Biology
- Stem Cell Research
Background:
- Triple-negative breast cancer (TNBC) lacks ER, PR, and HER2 expression, leading to poor prognosis and limited treatment options.
- Cancer stem cells (CSCs) drive tumor initiation, metastasis, recurrence, and drug resistance in TNBC.
- Targeting CSCs is a promising strategy to overcome TNBC's aggressive nature.
Purpose of the Study:
- To review compounds targeting cell signaling pathways crucial for TNBC stem cell survival and self-renewal.
- To explore potential therapeutic strategies for eradicating TNBC stem cells.
Main Methods:
- Literature review of compounds targeting specific cell signaling pathways.
- Focus on pathways including Hedgehog, NF-κB, Wnt, Notch, Hippo, TGF-β, JAK/STAT, and PI3K/AKT/mTOR.
- Analysis of their role in TNBC stem cell biology.
Main Results:
- Several cell signaling pathways (Hedgehog, NF-κB, Wnt, Notch, Hippo, TGF-β, JAK/STAT, PI3K/AKT/mTOR) are critical for TNBC CSCs.
- Inhibitors of these pathways show potential for TNBC stem cell eradication.
- Targeting these pathways may overcome treatment resistance and improve outcomes.
Conclusions:
- Targeting cell signaling pathways offers a promising therapeutic avenue for TNBC.
- Inhibiting CSCs via these pathways could lead to more effective treatments for triple-negative breast cancer.
- Further research into these targeted therapies is warranted for clinical translation.
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