Journal
BMC CANCER
Volume 19, Issue -, Pages -Publisher
BMC
DOI: 10.1186/s12885-019-5839-2
Keywords
CRISPR; Cas9; microRNA; Breast cancer
Categories
Funding
- Oklahoma Center for the Advancement of Science and Technology [HR14-147, HR17-052]
- National Institute of General Medical Sciences of the National Institutes of Health [U54GM104938]
- Presbyterian Health Foundation
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BackgroundAltered expression of microRNAs (miRNAs) is known to contribute to cancer progression. miR-23b and miR-27b, encoded within the same miRNA cluster, are reported to have both tumor suppressive and oncogenic activity across human cancers, including breast cancer.MethodsTo clarify this dichotomous role in breast cancer, miR-23b and miR-27b were knocked out using CRISPR/Cas9 gene knockout technology, and the role of endogenous miR-23b and miR-27b was examined in a breast cancer model system in vitro and in vivo.ResultsCharacterization of the knockout cells in vitro demonstrated that miR-23b and miR-27b are indeed oncogenic miRNAs in MCF7 breast cancer cells. miR-23b and miR-27b knockout reduced tumor growth in xenograft nude mice fed a standard diet, supporting their oncogenic role in vivo. However, when xenograft mice were provided a fish-oil diet, miR-27b depletion, but not miR-23b depletion, compromised fish-oil-induced suppression of xenograft growth, indicating a context-dependent nature of miR-27b oncogenic activity.ConclusionsOur results demonstrate that miR-23b and miR-27b are primarily oncogenic in MCF7 breast cancer cells and that miR-27b may have tumor suppressive activity under certain circumstances.
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