Abstract
Breast cancer stem cells (BCSCs) are the minor population of breast cancer (BC) cells that exhibit several phenotypes such as migration, invasion, self-renewal, and chemotherapy as well as radiotherapy resistance. Recently, BCSCs have been more considerable due to their capacity for recurrence of tumors after treatment. Recognition of signaling pathways and molecular mechanisms involved in stemness phenotypes of BCSCs could be effective for discovering novel treatment strategies to target BCSCs. This review introduces BCSC markers, their roles in stemness phenotypes, and the dysregulated signaling pathways involved in BCSCs such as mitogen-activated protein (MAP) kinase, PI3K/Akt/nuclear factor kappa B (NFκB), TGF-β, hedgehog (Hh), Notch, Wnt/β-catenin, and Hippo pathway. In addition, this review presents recently discovered molecular mechanisms implicated in chemotherapy and radiotherapy resistance, migration, metastasis, and angiogenesis of BCSCs. Finally, we reviewed the role of microRNAs (miRNAs) in BCSCs as well as several other therapeutic strategies such as herbal medicine, biological agents, anti-inflammatory drugs, monoclonal antibodies, nanoparticles, and microRNAs, which have been more considerable in the last decades.
Highlights
The most common cancer among women all over the world is breast cancer (BC)
We have summarized the malignant characterization of breast cancer stem cells (BCSCs) such as drug and radiotherapy resistance, metastasis and References miR-10b miR-21
The contribution of Wnt signaling in stemness phenotypes of Cancer stem cells (CSCs) is mediated by programmed death 1 (PD-1), which is overexpressed in BCSCs
Summary
It has been noted that a number of signaling pathways including MAP kinase, PI3K/Akt/NFκB, TGF-β, hedgehog (Hh), Notch, Wnt/β-catenin, and Hippo signaling have been implicated in stemness maintenance and regulation of selfrenewal, metastasis, and therapeutic resistance into CSCs [12, 14, 56,57,58,59,60,61]. The contribution of Wnt signaling in stemness phenotypes of CSCs is mediated by programmed death 1 (PD-1), which is overexpressed in BCSCs. In addition, Wnt activators and Wnt inhibitors upand down-regulate PD-1, respectively.
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