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
. 2022 Jun 4;9(6):245.
doi: 10.3390/bioengineering9060245.

Contribution of Tumor-Derived Extracellular Vesicles to Malignant Transformation of Normal Cells

Affiliations
Review

Contribution of Tumor-Derived Extracellular Vesicles to Malignant Transformation of Normal Cells

Daria S Chulpanova et al. Bioengineering (Basel). .

Abstract

Tumor-cell-derived extracellular vesicles (EVs) are known to carry biologically active molecules of parental cells, which can actively modulate the tumor microenvironment. EVs produced by tumor cells play significant roles in the development and maintenance of tumor growth, metastasis, immune escape, and other important processes. However, the ability of EVs to induce the transformation of normal cells has hardly been investigated. This review discusses studies that describe the ability of tumor-cell-derived EVs to alter the metabolism and morphology of normal cells, causing changes associated with malignant transformation. Additionally, the horizontal transfer of oncogenes through EVs of tumor cells and the induction of epigenetic changes in normal cells, which leads to genomic instability and subsequent oncogenic transformation of normal cells, are also discussed.

Keywords: carcinogenesis; extracellular vesicles; tumor heterogeneity; tumor microenvironment.

PubMed Disclaimer

Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
The influence of tumor-cell-derived extracellular vesicle on the metabolism, structure, and epigenetic profile of normal cells.

Similar articles

Cited by

References

    1. Vogelstein B., Papadopoulos N., Velculescu V.E., Zhou S., Diaz L.A., Jr., Kinzler K.W. Cancer genome landscapes. Science. 2013;339:1546–1558. doi: 10.1126/science.1235122. - DOI - PMC - PubMed
    1. Parsa N. Environmental factors inducing human cancers. Iran. J. Public Health. 2012;41:1–9. - PMC - PubMed
    1. Mertz T.M., Harcy V., Roberts S.A. Risks at the DNA Replication Fork: Effects upon Carcinogenesis and Tumor Heterogeneity. Genes. 2017;8:46. doi: 10.3390/genes8010046. - DOI - PMC - PubMed
    1. Chen W.X., Liu X.M., Lv M.M., Chen L., Zhao J.H., Zhong S.L., Ji M.H., Hu Q., Luo Z., Wu J.Z., et al. Exosomes from Drug-Resistant Breast Cancer Cells Transmit Chemoresistance by a Horizontal Transfer of MicroRNAs. PLoS ONE. 2014;9:e95240. doi: 10.1371/journal.pone.0095240. - DOI - PMC - PubMed
    1. Li S., Zhou J., Wu H., Lu Q., Tai Y., Liu Q., Wang C. Oncogenic transformation of normal breast epithelial cells co-cultured with cancer cells. Cell Cycle. 2018;17:2027–2040. doi: 10.1080/15384101.2018.1511510. - DOI - PMC - PubMed

LinkOut - more resources