miR-141-3p Regulates the Proliferation and Apoptosis of Endometrial-Myometrial Interface Smooth Muscle Cells in Adenomyosis Via JAK2/STAT3 Pathway

Sirui Wang, Hua Duan, Sha Wang, Zhengchen Guo, Qi Lin
Biochemical genetics · 2023 · vol. 62(3) , pp. 2049–2065 · doi:10.1007/s10528-023-10508-4 · PMID:37828348 · W4387580260
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⚙ AI-generated summary by claude@2026-06+body, 2026-06-07 ⓘ

This study found that miR-141-3p levels were decreased in adenomyosis smooth muscle cells, and its overexpression inhibited proliferation and enhanced apoptosis via the JAK2/STAT3 pathway.

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⚙ AI-generated deep summary by claude@2026-06, 2026-06-07 ⓘ

This paper investigated how miR-141-3p influences proliferation and apoptosis of smooth muscle cells (SMCs) derived from the endometrial-myometrial interface in adenomyosis, using EMI tissue cultures from 25 patients with adenomyosis and 20 without. The authors measured miR-141-3p and JAK2/STAT3 (including phosphorylated forms) by RT-qPCR and western blot, then assessed cell proliferation via CCK-8 and apoptosis by flow cytometry after manipulating miR-141-3p with mimics/inhibitors and blocking JAK2/STAT3 signaling with the inhibitor WP1066. They found miR-141-3p was decreased while JAK2 and STAT3 were increased in adenomyosis EMI SMCs; miR-141-3p overexpression inhibited proliferation and promoted apoptosis, and WP1066 produced effects consistent with reduced JAK2/STAT3 activity, with rescue experiments supporting JAK2/STAT3 as a downstream pathway of miR-141-3p. The primary limitation is that the work is based on primary cultured cells and pathway modulation rather than in vivo or clinical outcome validation. This paper is centrally about adenomyosis — it specifically analyzes miR-141-3p regulation of EMI smooth muscle cell proliferation and apoptosis through the JAK2/STAT3 pathway.

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Abstract

Adenomyosis (ADS) is a common benign gynecological disease. Abnormal proliferation at the endometrial-myometrial interface (EMI) plays a crucial role in the occurrence and progression of ADS. miR-141-3p is associated with cell proliferation and apoptosis. However, the specific mechanism of miR-141-3p in the etiology of ADS is still unknown. In this study, we explored the effects of miR-141-3p on the proliferation and apoptosis of ADS EMI smooth muscle cells (SMCs). We collected EMI tissues for the primary culture of SMCs from 25 patients diagnosed with ADS and 20 without ADS. Real-time quantitative polymerase chain reaction and western blot were used to measure the mRNA and protein expression levels of miR-141-3p, JAK2, STAT3, phospho-JAK2, and phospho-STAT3 in ADS EMI SMCs. The cell counting kit 8 assay and flow cytometry analysis were used to evaluate the proliferation and apoptosis of EMI SMCs. The miR-141-3p mimic/inhibitor was used to increase or decrease the expression level of miR-141-3p. We added WP1066 to block the phosphorylation of JAK2/STAT3 pathway components. The miR-141-3p levels were decreased, while JAK2 and STAT3 levels were increased in ADS EMI SMCs. miR-141-3p overexpression significantly inhibited the proliferation and enhanced the apoptosis of EMI SMCs, whereas a decrease in miR-141-3p expression level was connected to the opposite results. Meanwhile, inactivated JAK2/STAT3 pathway decreased proliferation and enhanced apoptosis of EMI SMCs after WP1066 treatment. Furthermore, rescue experiments confirmed that the JAK2/STAT3 pathway was the downstream pathway of miR-141-3p and reduced the effect of miR-141-3p on the proliferation and apoptosis of EMI SMCs. These results demonstrate that miR-141-3p regulates the proliferation and apoptosis of ADS EMI SMCs by modulating the JAK2/STAT3 pathway.

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Condition tags

adenomyosis

MeSH descriptors

Adenomyosis Adenomyosis Adenomyosis Adenomyosis Adenomyosis Adenomyosis Adenomyosis Adenomyosis Adenomyosis Adenomyosis Adenomyosis Apoptosis Apoptosis Apoptosis Apoptosis Apoptosis Apoptosis Apoptosis Apoptosis Cell Proliferation

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