For immune check-point inhibitors to work, a tumor must be “hot” — that is, visible to the immune system. MiR-181a regulates a protein called STING, which plays an important role in innate immunity, and thus it may aid in making these tumors more responsive to immunotherapy.
“We’re currently working with collaborators in U-M’s drug discovery cores to identify small-molecules that might be able to modulate miR-181a, and therefore turn these ‘cold’ tumors ‘hot,’” she says.
Additionally, the findings may have relevance for other types of cancer, including breast cancer, prostate cancer and lung cancer, DiFeo notes. An analysis of more than 10,000 tumors across 38 different cancers in The Cancer Genome Atlas found higher levels of miR-181a were associated with worse outcomes for patients.
“This is significant because we found that miR-181a overexpression alone is sufficient to promote transformation of cells into cancer cells and to form tumors in mouse models,” DiFeo says.
The research continues in laboratory models with the goal of ultimately identifying drug compounds to advance toward human clinical trials.
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Additional authors on the study include: Matthew Knarr, of U-M and Case Western; Rita Avelar, Sreeja Sekhar, Michele Dziubinski, Jessica McAnulty and Stephanie Skala, of U-M; Lily J. Kwiatkowski and Stefanie Avril, of Case Western; and Ronny Drapkin of the University of Pennsylvania.
The research was supposed by grants from the National Cancer Institute (R01CA197780, P50CA159981), Department of Defense (OC150553), the Young Scientist Foundation and, as well as by donors and foundations including Norma and Al Gellar, the Silver Family Foundation and the Jacqueline E Bayley (JEB) Foundation.
Paper cited: “miR-181a initiates and perpetuates oncogenic transformation through the regulation of innate immune signaling,” Nature Communications. DOI: 10.1038/s41467-020-17030-w
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