Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2016 Sep;95(1 Suppl 1):S20-S25.
doi: 10.1097/MD.0000000000004766.

Cancer stem cells: Role in tumor growth, recurrence, metastasis, and treatment resistance

Jenny C Chang  1
Affiliations
Review

Cancer stem cells: Role in tumor growth, recurrence, metastasis, and treatment resistance

Jenny C Chang. Medicine (Baltimore). 2016 Sep.

Abstract

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.

PubMed Disclaimer

Conflict of interest statement

The author reports no conflicts of interest.

Figures

Figure 1
Figure 1
Epithelial-mesenchymal transition.[8,9]
Figure 2
Figure 2
Models of CSC-driven tumor heterogeneity.[16] CSC = cancer stem cell.
See this image and copyright information in PMC

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

References

    1. Ajani JA, Song S, Hochster HS, et al. Cancer stem cells: the promise and the potential. Semin Oncol 2015; 42 (suppl 1):S3–S17. - PubMed
    1. Chen K, Huang YH, Chen JL. Understanding and targeting cancer stem cells: therapeutic implications and challenges. Acta Pharmacol Sin 2013; 34:732–740. - PMC - PubMed
    1. Doherty MR, Smigiel JM, Junk DJ, et al. Cancer stem cell plasticity drives therapeutic resistance. Cancers (Basel) 2016; 8:pii: E8. - PMC - PubMed
    1. Takaishi S, Okumura T, Tu S, et al. Identification of gastric cancer stem cells using the cell surface marker CD44. Stem Cells 2009; 27:1006–1020. - PMC - PubMed
    1. Smith LM, Nesterova A, Ryan MC, et al. CD133/prominin-1 is a potential therapeutic target for antibody-drug conjugates in hepatocellular and gastric cancers. Br J Cancer 2008; 99:100–109. - PMC - PubMed

MeSH terms