The Role of Breast Cancer Stem Cells in Chemoresistance and Metastasis in Triple-Negative Breast Cancer

He, Lin; Wick, Neda; Germans, Sharon Koorse; Peng, Yan

doi:10.3390/cancers13246209

Cited by 39 publications

(24 citation statements)

References 120 publications

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“…Recent articles have reviewed the importance of CSCs in TNBC progression and therapeutic resistance [ 18 , 19 , 20 , 21 , 22 , 23 ]. TNBCs are enriched with CD44+/CD24−/ALDH1+ CSCs that contribute to metastases, chemoresistance and poor clinical outcomes [ 24 , 25 , 26 , 27 , 28 ].…”

Section: Introductionmentioning

confidence: 99%

“…Activation of Sonic Hedgehog (SHH) has also been identified as a pathway that contributes to the TNBC CSC state [ 33 , 34 , 35 ]. Agents that target WNT, NF-κB, NOTCH and SHH signaling are under development to eliminate CSCs in TNBCs, as well as other cancers [ 20 , 21 ]. Along these lines, small molecule inhibitors of WNT/β-catenin/TCF signaling are being developed based on their inhibition of TNBC CSCs in cell line and tumor models [ 36 , 37 , 38 ].…”

Section: Introductionmentioning

confidence: 99%

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Addiction of Cancer Stem Cells to MUC1-C in Triple-Negative Breast Cancer Progression

Yamashita

Küfe

2022

IJMS

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Triple-negative breast cancer (TNBC) is an aggressive malignancy with limited treatment options. TNBC progression is associated with expansion of cancer stem cells (CSCs). Few insights are available regarding druggable targets that drive the TNBC CSC state. This review summarizes the literature on TNBC CSCs and the compelling evidence that they are addicted to the MUC1-C transmembrane protein. In normal epithelia, MUC1-C is activated by loss of homeostasis and induces reversible wound-healing responses of inflammation and repair. However, in settings of chronic inflammation, MUC1-C promotes carcinogenesis. MUC1-C induces EMT, epigenetic reprogramming and chromatin remodeling in TNBC CSCs, which are dependent on MUC1-C for self-renewal and tumorigenicity. MUC1-C-induced lineage plasticity in TNBC CSCs confers DNA damage resistance and immune evasion by chronic activation of inflammatory pathways and global changes in chromatin architecture. Of therapeutic significance, an antibody generated against the MUC1-C extracellular domain has been advanced in a clinical trial of anti-MUC1-C CAR T cells and in IND-enabling studies for development as an antibody–drug conjugate (ADC). Agents targeting the MUC1-C cytoplasmic domain have also entered the clinic and are undergoing further development as candidates for advancing TNBC treatment. Eliminating TNBC CSCs will be necessary for curing this recalcitrant cancer and MUC1-C represents a promising druggable target for achieving that goal.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Addiction of Cancer Stem Cells to MUC1-C in Triple-Negative Breast Cancer Progression

Yamashita

Küfe

2022

IJMS

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“…Furthermore, cancer stroma cells use Warburg metabolism, whereas cancer stem cells’ metabolism is driven by mitochondrial oxidation [ 33 ]. In breast cancer, there are two types of cancer stem cells: CD44+/CD24 mesenchymal-like cancer stem cells and aldehyde dehydrogenase 1 family, member A1 (ALDH1) positive epithelial-like cancer stem cells [ 34 ]. Inhibiting mitochondrial oxidation can increase the proportion of cancer stroma to stem cells, allowing conventional chemotherapy to be more effective against stromal cells.…”

Section: Immunometabolismmentioning

confidence: 99%

Drug Metabolism for the Identification of Clinical Biomarkers in Breast Cancer

Costa

Vale

2022

IJMS

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Breast cancer is classified into four major molecular subtypes, and is considered a heterogenous disease. The risk profiles and treatment of breast cancer differ according to these subtypes. Early detection dramatically improves the prospects of successful treatment, resulting in a reduction in overall mortality rates. However, almost 30% of women primarily diagnosed with the early-stage disease will eventually develop metastasis or resistance to chemotherapies. Immunotherapies are among the most promising cancer treatment options; however, long-term clinical benefit has only been observed in a small subset of responding patients. The current strategies for diagnosis and treatment rely heavily on histopathological examination and molecular diagnosis, disregarding the tumor microenvironment and microbiome involving cancer cells. In this review, we aim to praise the use of pharmacogenomics and pharmacomicrobiomics as a strategy to identify potential biomarkers for guiding and monitoring therapy in real-time. The finding of these biomarkers can be performed by studying the metabolism of drugs, more specifically, immunometabolism, and its relationship with the microbiome, without neglecting the information provided by genetics. A larger understanding of cancer biology has the potential to improve patient care, enable clinical decisions, and deliver personalized medicine.

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“…Moreover, we further evaluated the effects of Dicer on the cell migratory/ invasive abilities and found that Dicer silencing enhanced both cell migration and invasion (Figure 3B). In addition, cancer stemness is a primary driver of cancer recurrence and metastasis [24][25][26]. Therefore, we surmised that Dicer participates in regulating the CSCs properties of breast cancer cells.…”

Section: Inhibition Of Dicer Expression Promotes the Migration Invasi...mentioning

confidence: 99%

Dicer-mediated miR-200b expression contributes to cell migratory/invasive abilities and cancer stem cells properties of breast cancer cells

Hsu

Chen

Liao

et al. 2022

Aging

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Distant metastasis is the leading cause of death in patients with breast cancer. Despite considerable treatment advances, the clinical outcomes of patients with metastatic breast cancer remain poor. CSCs can self-renew, enhancing cancer progression and metastasis. Dicer, a microRNA (miRNA) processing–related enzyme, is required for miRNA maturation. Imbalanced Dicer expression may be pivotal in cancer progression. However, whether and how Dicer affects the stemness of metastatic breast cancer cells remains unclear. Here, we hypothesized that Dicer regulates the migration, invasion, and stemness of breast cancer cells. We established highly invasive cell lines (MCF-7/I-3 and MDA-MB-231/I-3) and observed that Dicer expression was conspicuously lower in the highly invasive cells than in the parental cells. The silencing of Dicer significantly enhanced the cell migratory/invasive abilities and CSCs properties of the breast cancer cells. Conversely, the overexpression of Dicer in the highly invasive cells reduced their migration, invasion, and CSCs properties. Our bioinformatics analyses demonstrated that low Dicer levels were correlated with increased breast cancer risk. Suppression of Dicer inhibited miR-200b expression, whereas miR-200b suppression recovered Dicer knockdown–induced migration, invasion, and cancer stem cells (CSCs) properties of the breast cancer cells. Thus, our findings reveal that Dicer is a crucial regulator of the migration, invasion, and CSCs properties of breast cancer cells and is significantly associated with poor survival in patients with breast cancer.

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The Role of Breast Cancer Stem Cells in Chemoresistance and Metastasis in Triple-Negative Breast Cancer

Cited by 39 publications

References 120 publications

Addiction of Cancer Stem Cells to MUC1-C in Triple-Negative Breast Cancer Progression

Addiction of Cancer Stem Cells to MUC1-C in Triple-Negative Breast Cancer Progression

Drug Metabolism for the Identification of Clinical Biomarkers in Breast Cancer

Dicer-mediated miR-200b expression contributes to cell migratory/invasive abilities and cancer stem cells properties of breast cancer cells

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