micro RNA Let‐7b: A Novel treatment for endometriosis

Cagdas Sahin, Çağdaş Şahin, Ramanaiah Mamillapalli, Kyong Wook Yi, Kyong W Yi, Hugh S Taylor
Journal of cellular and molecular medicine · 2018 · vol. 22(11) , pp. 5346–5353 · doi:10.1111/jcmm.13807 · PMID:30063121 · PMC6201226 · W2886983271
article OA: gold CC0 ⤵ 39 in-corpus citations
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This study demonstrates that local treatment of endometriosis lesions with microRNA Let-7b in a murine model reduces lesion size by downregulating genes involved in estrogen signaling, inflammation, and growth factor receptors.

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Abstract

Endometriosis is an oestrogen-dependent, chronic inflammatory disease that affects 10% of reproductive-aged women. Current treatment options depend on female sex steroid hormone modulation; however, all have side effects and are not useful in women who want to conceive. microRNAs treatments have provided promising results for some chronic diseases and cancers. We have previously shown the microRNA Let-7b is repressed in endometriosis and that loss of Let-7 contributes to the pathophysiology of the disease. Here, we propose using microRNA Let-7b for the treatment of endometriosis in a murine model. Endometriosis was treated using microRNA Let-7b or a scrambled control microRNA. Let-7b treatment resulted in reduced endometriosis lesion size. Decreased gene expression was noted in several genes known to promote endometriosis growth including ER-α, ER-ß, Cyp19a, KRAS 4A, KRAS 4B and IL-6. These results indicate that microRNA Let-7b has a pleiotropic role in endometriosis pathophysiology affecting oestrogen signalling, inflammation and growth factor receptors. Local treatment of endometriosis with Let-7b is a promising therapy for endometriosis that simultaneously affects multiple pathways driving endometriosis without systemic hormonal side effects.

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Condition tags

endometriosis

MeSH descriptors

Endometriosis Inflammation MicroRNAs Animals Aromatase Aromatase Disease Models, Animal Endometriosis Endometriosis Endometriosis Estrogen Receptor alpha Estrogen Receptor alpha Estrogen Receptor beta Estrogen Receptor beta Female Gene Expression Regulation Humans Inflammation Inflammation Inflammation

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Cited by (39)

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