Abstract
Cancer stem cells (CSCs) are characterized by intrinsic self-renewal and tumorigenic properties, and play important roles in tumor initiation, progression, and resistance to diverse forms of anticancer therapy. Accordingly, targeting signaling pathways that are critical for CSC maintenance and biofunctions, including the Wnt, Notch, Hippo, and Hedgehog signaling cascades, remains a promising therapeutic strategy in multiple cancer types. Furthermore, advances in various cancer omics approaches have largely increased our knowledge of the molecular basis of CSCs, and provided numerous novel targets for anticancer therapy. However, the majority of recently identified targets remain ‘undruggable’ through small-molecule agents, whereas the implications of exogenous RNA interference (RNAi, including siRNA and miRNA) may make it possible to translate our knowledge into therapeutics in a timely manner. With the recent advances of nanomedicine, in vivo delivery of RNAi using elaborate nanoparticles can potently overcome the intrinsic limitations of RNAi alone, as it is rapidly degraded and has unpredictable off-target side effects. Herein, we present an update on the development of RNAi-delivering nanoplatforms in CSC-targeted anticancer therapy and discuss their potential implications in clinical trials.
Highlights
Published: 8 December 2021Cancer is one of the leading causes of poor quality of life and mortality worldwide [1,2].Currently, most cancer patients have micro- or macroscopic systemic metastases when they are initially diagnosed [1]
The results suggested that the antitumor effect of exosome-mimetic nanoparticles Raw264.7NVDox was significantly greater than conventional chemotherapeutic-loaded nanoparticles [186,187]
The Cancer stem cells (CSCs) hypothesis posits that CSCs are greatly responsible for tumor heterogeneity, tumorigenesis, and therapy resistance, having an important role in cancer initiation and progression [14,25]
Summary
Cancer is one of the leading causes of poor quality of life and mortality worldwide [1,2]. New therapeutic strategies, including targeted therapies and immunotherapy, have been proposed [6,7], cancer resistance continues to emerge by similar mechanisms [8,9,10]. The CSC phenotype exhibits increased resistance to chemotherapy, by raising drug efflux and by regulating many other stem characteristics, including upregulated antiapoptotic proteins and increased DNA damage repair ability [25]. In this context, several signaling pathways and malignant molecules are critical in stemness maintenance, such as the Wnt and Notch pathways, and the NF-E2-Related Factor 2 (NRF2), CD44, prominin.
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