miR-92a promotes progesterone resistance in endometriosis through PTEN/AKT pathway

Manchao Li, Peng J, Jintao Peng, Yanan Shi, Shi Y, Peng Sun, Sun P
Life sciences · 2019 · vol. 242 , pp. 117190 · doi:10.1016/j.lfs.2019.117190 · PMID:31863773 · W2996245516
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MicroRNA-92a enhances progesterone resistance in endometriosis by inhibiting PTEN, leading to increased AKT phosphorylation.

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Abstract

The alteration of PTEN expression may be a vital part of the pathological and physiological mechanisms in infertility-related with endometriosis. However, the potential mechanisms underlying abnormal expression of PTEN and its role in progesterone-resistant endometriosis have not been thoroughly elucidated. In this study, our data showed the PTEN messenger RNA (mRNA) level and protein expression was reduced in progesterone-resistant endometriosis tissue and primary stomal cells. Low levels of PTEN in endometrial stromal cells led to higher cell proliferation and resistance to progesterone. In terms of PTEN suppression in progesterone-resistant endometriosis, the mRNA level of miR-92a was correlated negatively with PTEN level. Transfection of miR-92a mimic reduced PTEN expression and made the stromal cells more resistant to progesterone treatment. Inhibition of miR-92a by its antagomir had the opposite effects. Results of the luciferase reporter assay for the 3'-nontranslated region suggested that miR-92a directly modulated PTEN levels. Moreover, miR-92a inhibition by its antagomir enhanced the therapeutic effect of progesterone, which suppressed stromal cell proliferation, and reduced the formation of ectopic lesions in the mouse model of endometriosis. Hence, this study revealed that miR-92a contributed to the development of progesterone resistant endometriosis by suppression of PTEN expression, and modulation of miR-92a might be a potential medical method of treating endometriosis.

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Condition tags

endometriosis

MeSH descriptors

Endometriosis MicroRNAs Progesterone Proto-Oncogene Proteins c-akt PTEN Phosphohydrolase Signal Transduction Adult Animals Cells, Cultured Disease Models, Animal Drug Resistance Endometriosis Endometriosis Female Humans Immunoblotting Mice MicroRNAs MicroRNAs Progesterone

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