Correction: Expression of lncRNA NEAT1 in endometriosis and its biological functions in ectopic endometrial cells as mediated via miR-124-3p

Genes & genomics · 2025 · vol. 47(12) , pp. 1389–1391 · doi:10.1007/s13258-025-01651-w · PMID:40676493
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This correction article addresses the expression of lncRNA NEAT1 in endometriosis and its biological functions in ectopic endometrial cells as mediated via miR-124-3p.

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This notice is a correction to a previously published article in Genes & Genomics (2022) that investigated lncRNA NEAT1 in endometriosis and its biological functions in ectopic endometrial cells mediated via miR-124-3p. The authors state that Fig. 4 was incorrectly published, and they provide the corrected version describing NEAT1 silencing effects in endometrial stromal cells extracted from ectopic endometrium of patients with endometriosis, including measures of cell viability (MTT), apoptosis by flow cytometry, caspase-3 activity, and protein changes in Bax and Bcl-2 with reference to miR-124-3p regulation. The correction does not report new experimental results beyond replacing the figure. This paper is centrally about endometriosis — it specifically concerns the corrected presentation of how NEAT1 silencing affects proliferation and apoptosis in ectopic endometrial stromal cells via miR-124-3p.

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CORRECTION Genes & Genomics (2025) 47:1389–1391 https://doi.org/10.1007/s13258-025-01651-w Correction to: Genes & Genomics (2022) 44:527–537 h t t p s : / / d o i . o r g / 1 0 . 1 0 0 7 / s 1 3 2 5 8 - 0 2 1 - 0 1 1 8 4 - y In the original version of this article, Fig. 4 were incorrectly published. Donglan Yuan and Dandan Zhu contributed equally. The original article can be found online at h t t p s : / / d o i . o r g / 1 0 . 1 0 0 7 / s 1 3 2 5 8 - 0 2 1 - 0 1 1 8 4 - y. Hua Qian [email protected] 1 Department of Obstetrics and Gynecology, Taizhou People’s Hospital Afliated to Nantong University, 399 Hailing Road, Taizhou 225300, People’s Republic of China 2 Department of Operation, Taizhou People’s Hospital Afliated to Nantong University, Taizhou 225300, China Published online: 17 July 2025 © The Author(s) under exclusive licence to The Genetics Society of Korea 2025 Correction: Expression of lncRNA NEAT1 in endometriosis and its biological functions in ectopic endometrial cells as mediated via miR- 124-3p Donglan Yuan1 · Dandan Zhu1 · Boyu Yin1 · Hongshan Ge1 · Yinling Zhao1 · Aihua Huang1 · Xiaosu Wang1 · Xiuhong Cao2 · Nan Xia1 · Hua Qian1 1 3 Online ISSN 2092-9293 Print ISSN 1976-9571 Genes & Genomics (2025) 47:1389–1391 Incorrect Version of Fig. 4: Fig. 4 NEAT1 silencing inhibits proliferation, but promotes apoptosis, in EC-ESCs by negatively regulating miR-124-3p expression. A Cell viability evaluated by MTT assay. B Flow cytometric analysis was employed to detect the levels of cell apoptosis. C Statistics of apop - tosis rate. D Caspase-3 activity in EC-ESCs following transfection. E Efects of NEAT1 and miR-124-3p on the protein expression levels of Bax and Bcl-2. F The Bax/Bcl-2 ratio is shown. EC-ESCs, endometrial stromal cells extracted from ectopic endometrium from patients with EM; EM endometriosis; NEAT1 nuclear paraspeckle assembly tran - script 1; miR microRNA Fig. 4 NEAT1 silencing inhibits proliferation, but promotes apoptosis, in EC-ESCs by negatively regulating miR-124-3p expression. A Cell viability evaluated by MTT assay. B Flow cytometric analysis was employed to detect the levels of cell apoptosis. C Statistics of apop - tosis rate. D Caspase-3 activity in EC-ESCs following transfection. E Efects of NEAT1 and miR-124-3p on the protein expression levels of Bax and Bcl-2. F The Bax/Bcl-2 ratio is shown. EC-ESCs, endometrial stromal cells extracted from ectopic endometrium from patients with EM; EM endometriosis; NEAT1 nuclear paraspeckle assembly tran - script 1; miR microRNA Correct Version of Fig. 4: 1 3 1390 Genes & Genomics (2025) 47:1389–1391 The original article has been corrected. Publisher’s note Springer Nature remains neutral with regard to juris- dictional claims in published maps and institutional affiliations. 1 3 1391

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