This study aimed to explore whether exosome-derived circ0009910 can transcellularly regulate the growth of pituitary adenoma (PA) cells and to further explore the possible mechanisms of its action.
MethodsTransmission electron microscopy and nanoparticle size analysis were used to observe the morphology and size of the exosomes. Real-time quantitative polymerase chain reaction (qRT-PCR) was used to determine the expression of circ_0009910, miR-106b-5p, and signal transducer and activator of transcription3 (STAT3). Western blotting was used to assess the expression of exosomal marker proteins, p-STAT3, E-cadherin, N-cadherin, and vimentin. Cell Counting Kit-8 (CCK-8) and 5-Ethynyl-2-deoxyuridine (EdU) assays were used to determine the proliferative capacity of the cells. Transwell assays were performed to assess the migratory and invasive capacity of the cells. Enzyme-linked immunosorbent assays (ELISAs) were used to determine the expression level of growth hormone (GH). A nude mouse xenograft model was established to observe the effects of exosome-derived circ0009910 on transplanted tumors in nude mice.
Resultscirc0009910 can be transferred to other cells via exosomes. Knocking down the expression of circ0009910 can inhibit the proliferation, invasion, and migration of PA cells, reduce GH expression, and regulate the expression of epithelial–mesenchymal transition (EMT)-associated proteins. miR-106b-5p is a molecular sponge of circ0009910 and can partially reverse the procarcinogenic effect of circ0009910 in PA. STAT3 is a target gene of miR-106b-5p. In addition, circ0009910 knockdown inhibited tumor growth in vivo.
ConclusionExosome-derived circ0009910 promotes PA progression and regulates EMT through the miR-106b-5p/STAT3 axis.
Keywords pituitary adenoma - exosomes - circ0009910 - invasion*These authors contributed equally to this article.
Received: 17 March 2024
Accepted: 13 March 2025
Accepted Manuscript online:
05 May 2025
Article published online:
18 September 2025
© 2025. The Author(s). This is an open access article published by Thieme under the terms of the Creative Commons Attribution License, permitting unrestricted use, distribution, and reproduction so long as the original work is properly cited. (https://creativecommons.org/licenses/by/4.0/)
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