Cancer stem cells: Role in tumor growth, recurrence, metastasis, and treatment resistance
Open accessAbstract
Cancer stem cells (CSCs) are a class of pluripotent cells that have been observed in most types of solid and hematologic cancers. CSCs have been shown in numerous cancer models to be involved in tumor development, cell proliferation, and metastatic dissemination, while possessing a capacity for sustained self-renewal. CSCs, which typically represent a small proportion of total cells of a given tumor, also exhibit resistance to chemotherapy and radiotherapy. Indeed, exposure to these treatments may promote "stemness" in nonstem cancer cells, which may explain why successful therapeutic reduction of tumor bulk will often fail to produce clinical improvement. Acquisition of stemness involves epithelial-mesenchymal transition (EMT), in which epithelial cells are transformed into a mesenchymal phenotype characterized by increased capacities for migration, invasiveness, and resistance to apoptosis. EMT may also contribute to metastasis by driving dissemination of mesenchymal CSCs to distant locations, whereupon the CSCs revert to an epithelial phenotype to support metastatic tumor growth. Several different approaches to treatment aimed at overcoming the intrinsic resistance of CSCs to conventional therapies are currently being developed. These include agents targeting tumorigenic pathways, such as JAK2/STAT3 and PI3K/mTOR, and immunotherapies, including vaccines and natural killer cells employed to induce a T cell response.
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CSCs are a subpopulation of tumor cells with capacity for sustained self-renewal that can drive tumor initiation, relapses, metastasis, and resistance to therapy.
“CSCs are a subpopulation of tumor cells with the capacity for sustained self-renewal that, in turn, can not only drive tumor initiation but can also cause relapses, metastasis, and resistance to therapy [82,83].”
From 20-Hydroxyecdysone Confers Antioxidant and Antineoplastic Properties in Human Non-Small Cell Lung Cancer Cells (2023) · cites this paper as [83]
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- Authors
- Chang, J. C.
- Affiliations
- Houston Methodist (US)
- Corresponding author
- Chang, Jenny C.
- ORCID
- Chang, Jenny C.
- Venue
- Medicine
- Published
- 2016-09
- Volume
- 95
- Issue
- 1S
- Pages
- S20-S25
- ISSN
- 0025-7974 (ISSN-L)
- PMC
- PMC5599212
- OpenAlex
- W2512891139
- Cited by
- 435
- References
- 42
- Citations by year
- 2026: 17 · 2025: 34 · 2024: 62 · 2023: 68 · 2022: 75 · 2021: 60 · 2020: 43 · 2019: 42 · 2018: 22 · 2017: 10 · 2016: 2
- FWCI
- 2.55
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- cc-by-nc
- Locations
- Medicine (publishedVersion, cc-by-nc)
- Europe PMC (PubMed Central) (publishedVersion, cc-by-nc)
- PubMed Central (publishedVersion, cc-by-nc)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Oncology › Cancer Cells and Metastasis
- Health Sciences › Medicine › Genetics › Mesenchymal stem cell research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Developmental Biology and Gene Regulation
- Keywords
- cancer stem cells, self-renewal, chemoresistance, radiotherapy resistance, epithelial-mesenchymal transition, metastasis, stemness, JAK2/STAT3 signaling, PI3K/mTOR signaling, cancer immunotherapy, cancer vaccines, natural killer cells, tumor cell proliferation
- MeSH terms
- Humans, Neoplasm Metastasis, Neoplasm Recurrence, Local, Neoplasms, Neoplastic Stem Cells, Signal Transduction, Drug Resistance, Neoplasm, Epithelial-Mesenchymal Transition, Carcinogenesis
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