APEX1/miR-24 axis: a promising therapeutic target in endometriosis

review OA: closed public-domain-us
Full text JSON View on PubMed View at publisher
AI-generated summary by claude@2026-07, 2026-07-16

APEX1 and miR-24 were highly expressed in endometriosis tissues and promoted cell proliferation and inhibited apoptosis by upregulating miR-24 expression.

One-sentence paraphrase of the abstract; not a substitute for reading it. No clinical advice. How this works

AI-generated deep summary by claude@2026-07, 2026-07-16 · read from full text

This retracted study investigated aberrant APEX1 expression and its mechanism involving miR-24 in human endometrial stromal cells (ESC), using endometriosis tissue samples. APEX1 and miR-24 levels were measured by qRT-PCR and Western blot, and ESCs were genetically manipulated (APEX1 overexpression/knockdown and miR-24 mimic/inhibitor, including combinations) to assess proliferation and apoptosis. The authors reported that both APEX1 and miR-24 were highly expressed in endometriosis tissues and that increasing either factor promoted ESC proliferation while affecting apoptosis markers (increasing Bax and cleaved-caspase-3 and decreasing Bcl-2), with effects reversed by silencing APEX1 or miR-24; they also reported a positive correlation between APEX1 and miR-24, supported by an RNA immunoprecipitation assay for pri-miR-24/miR-24 interaction. A major caveat is that the article was later retracted, so its findings are not reliable, and the paper does not appear to provide additional corroboration beyond these assays. This paper is centrally about endometriosis — it specifically claims an APEX1/miR-24 axis that regulates endometrial stromal cell proliferation and apoptosis in endometriosis.

Read from the paper's body, not the abstract. Not a substitute for reading the paper. No clinical advice. How this works

Abstract

PURPOSE: The present work aimed to explore the aberrant expression of APEX1 in endometrial stromal cells (ESC) and the underlying mechanisms. METHODS: The levels of APEX1 and miR-24 in endometriosis tissues were tested by qRT-PCR and Western blot. After cell transfection, cells were correspondingly classified into pcDNA3.1-NC, sh-NC, mimic NC, inhibitor NC, pcDNA3.1-APEX1, sh-APEX1, miR-24 mimic, miR-24 inhibitor, sh-NC + inhibitor NC, inhibitor-NC + sh-APEX1, sh-NC + miR-24 inhibitor, pcDNA3.1-NC + mimic NC, mimic NC + pcDNA3.1-APEX1 and pcDNA3.1-NC + miR-24 mimic group. Besides, cell proliferation, apoptosis in addition to apoptosis-related proteins Bax, Bcl-2 and cleaved-casase-3 were analyzed by BrdU assay, flow cytometry (FCM) and Western blot assays, respectively. Additionally, RIP assay was conducted to determine the interaction between pri-miR-24 and miR-24. RESULTS: APEX1 and miR-24 were highly expressed in endometriosis tissues. Overexpression of APEX1 and miR-24 potentiates ESC proliferation and inhibits apoptosis, while those effects could be reversed by APEX1 and miR-24 silencing. Meanwhile, APEX1 and miR-24 could elevate ESC apoptosis-related proteins Bax and cleaved-caspase-3 and decrease Bcl-2 expression. Importantly, APEX1 was positively correlated with miR-24 expression. CONCLUSION: APEX1 promotes ESC proliferation and inhibits apoptosis by upregulating miR-24 expression.
Full text 11,359 characters · extracted from oa-doi-fallback · 5 sections · click to expand

Abstract

Purpose The present work aimed to explore the aberrant expression of APEX1 in endometrial stromal cells (ESC) and the underlying mechanisms.

Methods

The levels of APEX1 and miR-24 in endometriosis tissues were tested by qRT-PCR and Western blot. After cell transfection, cells were correspondingly classified into pcDNA3.1-NC, sh-NC, mimic NC, inhibitor NC, pcDNA3.1-APEX1, sh-APEX1, miR-24 mimic, miR-24 inhibitor, sh-NC + inhibitor NC, inhibitor-NC + sh-APEX1, sh-NC + miR-24 inhibitor, pcDNA3.1-NC + mimic NC, mimic NC + pcDNA3.1-APEX1 and pcDNA3.1-NC + miR-24 mimic group. Besides, cell proliferation, apoptosis in addition to apoptosis-related proteins Bax, Bcl-2 and cleaved-casase-3 were analyzed by BrdU assay, flow cytometry (FCM) and Western blot assays, respectively. Additionally, RIP assay was conducted to determine the interaction between pri-miR-24 and miR-24.

Results

APEX1 and miR-24 were highly expressed in endometriosis tissues. Overexpression of APEX1 and miR-24 potentiates ESC proliferation and inhibits apoptosis, while those effects could be reversed by APEX1 and miR-24 silencing. Meanwhile, APEX1 and miR-24 could elevate ESC apoptosis-related proteins Bax and cleaved-caspase-3 and decrease Bcl-2 expression. Importantly, APEX1 was positively correlated with miR-24 expression.

Conclusion

APEX1 promotes ESC proliferation and inhibits apoptosis by upregulating miR-24 expression. Similar content being viewed by others Data availability The datasets used or analyzed during the current study are available from the corresponding author on reasonable request. Change history 13 February 2026 This article has been retracted. Please see the Retraction Notice for more detail: https://doi.org/10.1007/s00404-026-08363-w

References

Hickey M, Ballard K, Farquhar C (2014) Endometriosis. BMJ 348:g1752. https://doi.org/10.1136/bmj.g1752 Vercellini P, Vigano P, Somigliana E, Fedele L (2014) Endometriosis: pathogenesis and treatment. Nat Rev Endocrinol 10(5):261–275. https://doi.org/10.1038/nrendo.2013.255 Laschke MW, Menger MD (2018) Basic mechanisms of vascularization in endometriosis and their clinical implications. Hum Reprod Update 24(2):207–224. https://doi.org/10.1093/humupd/dmy001 Rutherford EJ, Hill ADK, Hopkins AM (2018) Adhesion in physiological, benign and malignant proliferative states of the endometrium: microenvironment and the clinical big picture. Cells. https://doi.org/10.3390/cells7050043 Soni UK, Chadchan SB, Kumar V, Ubba V, Khan MTA, Vinod BSV, Konwar R, Bora HK, Rath SK, Sharma S, Jha RK (2019) A high level of TGF-B1 promotes endometriosis development via cell migration, adhesiveness, colonization, and invasivenessdagger. Biol Reprod 100(4):917–938. https://doi.org/10.1093/biolre/ioy242 Kim JM, Yeo MK, Lim JS, Song IS, Chun K, Kim KH (2019) APEX1 expression as a potential diagnostic biomarker of clear cell renal cell carcinoma and hepatobiliary carcinomas. J Clin Med. https://doi.org/10.3390/jcm8081151 Kim MH, Kim HB, Yoon SP, Lim SC, Cha MJ, Jeon YJ, Park SG, Chang IY, You HJ (2013) Colon cancer progression is driven by APEX1-mediated upregulation of Jagged. J Clin Invest. https://doi.org/10.1172/JCI65521 Antoniali G, Serra F, Lirussi L, Tanaka M, D’Ambrosio C, Zhang S, Radovic S, Dalla E, Ciani Y, Scaloni A, Li M, Piazza S, Tell G (2017) Mammalian APE1 controls miRNA processing and its interactome is linked to cancer RNA metabolism. Nat Commun 8(1):797. https://doi.org/10.1038/s41467-017-00842-8 Chen Y, Li J, Mo Z (2016) Association between the APEX1 Asp148Glu polymorphism and prostate cancer, especially among Asians: a new evidence-based analysis. Oncotarget 7(32):52530–52540. https://doi.org/10.18632/oncotarget.9693 Jiang S, Zhu L, Tang H, Zhang M, Chen Z, Fei J, Han B, Zou GM (2015) Ape1 regulates WNT/beta-catenin signaling through its redox functional domain in pancreatic cancer cells. Int J Oncol 47(2):610–620. https://doi.org/10.3892/ijo.2015.3048 Mahjabeen I, Baig RM, Sabir M, Kayani MA (2013) Genetic and expressional variations of APEX1 are associated with increased risk of head and neck cancer. Mutagenesis 28(2):213–218. https://doi.org/10.1093/mutage/ges074 Mohammed MZ, Vyjayanti VN, Laughton CA, Dekker LV, Fischer PM, Wilson DM 3rd, Abbotts R, Shah S, Patel PM, Hickson ID, Madhusudan S (2011) Development and evaluation of human AP endonuclease inhibitors in melanoma and glioma cell lines. Br J Cancer 104(4):653–663. https://doi.org/10.1038/sj.bjc.6606058 Hsu CM, Chang WS, Hwang JJ, Wang JY, Hsiao YL, Tsai CW, Liu JC, Ying TH, Bau DT (2014) The role of apurinic/apyrimidinic endonuclease DNA repair gene in endometriosis. Cancer Genomics Proteomics 11(6):295–301 Dai Y, Lin X, Xu W, Lin X, Huang Q, Shi L, Pan Y, Zhang Y, Zhu Y, Li C, Liu L, Zhang S (2019) MiR-210-3p protects endometriotic cells from oxidative stress-induced cell cycle arrest by targeting BARD1. Cell Death Dis 10(2):144. https://doi.org/10.1038/s41419-019-1395-6 Chen G, Chen Z, Zhao H (2020) MicroRNA-155-3p promotes glioma progression and temozolomide resistance by targeting Six1. J Cell Mol Med 24(9):5363–5374. https://doi.org/10.1111/jcmm.15192 Villanova L, Barbini C, Piccolo C, Boe A, De Maria R, Fiori ME (2020) miR-1285–3p controls colorectal cancer proliferation and escape from apoptosis through DAPK2. Int J Mol Sci. https://doi.org/10.3390/ijms21072423 Wang H, Lin X, Liu E, Jian Z, Ou Y (2020) MicroRNA-33b regulates hepatocellular carcinoma cell proliferation, apoptosis, and mobility via targeting Fli-1-mediated Notch1 pathway. J Cell Physiol. https://doi.org/10.1002/jcp.29673 Zhao J, Hu C, Chi J, Li J, Peng C, Yun X, Li D, Yu Y, Li Y, Gao M, Zheng X (2016) miR-24 promotes the proliferation, migration and invasion in human tongue squamous cell carcinoma by targeting FBXW7. Oncol Rep 36(2):1143–1149. https://doi.org/10.3892/or.2016.4891 Cai H, Zhu XX, Li ZF, Zhu YP, Lang JH (2018) MicroRNA Dysregulation and steroid hormone receptor expression in uterine tissues of rats with endometriosis during the implantation window. Chin Med J (Engl) 131(18):2193–2204. https://doi.org/10.4103/0366-6999.240808 Dong P, Ihira K, Xiong Y, Watari H, Hanley SJ, Yamada T, Hosaka M, Kudo M, Yue J, Sakuragi N (2016) Reactivation of epigenetically silenced miR-124 reverses the epithelial-to-mesenchymal transition and inhibits invasion in endometrial cancer cells via the direct repression of IQGAP1 expression. Oncotarget 7(15):20260–20270. https://doi.org/10.18632/oncotarget.7754 Liu H, Zhang Z, Xiong W, Zhang L, Xiong Y, Li N, He H, Du Y, Liu Y (2017) Hypoxia-inducible factor-1alpha promotes endometrial stromal cells migration and invasion by upregulating autophagy in endometriosis. Reproduction 153(6):809–820. https://doi.org/10.1530/REP-16-0643 Ballista-Hernandez J, Martinez-Ferrer M, Velez R, Climent C, Sanchez-Vazquez MM, Torres C, Rodriguez-Munoz A, Ayala-Pena S, Torres-Ramos CA (2017) Mitochondrial DNA integrity is maintained by APE1 in carcinogen-induced colorectal cancer. Mol Cancer Res 15(7):831–841. https://doi.org/10.1158/1541-7786.MCR-16-0218 Herring CJ, West CM, Wilks DP, Davidson SE, Hunter RD, Berry P, Forster G, MacKinnon J, Rafferty JA, Elder RH, Hendry JH, Margison GP (1998) Levels of the DNA repair enzyme human apurinic/apyrimidinic endonuclease (APE1, APEX, Ref-1) are associated with the intrinsic radiosensitivity of cervical cancers. Br J Cancer 78(9):1128–1133. https://doi.org/10.1038/bjc.1998.641 Sun Z, Zhu Y, Aminbuhe FQ, Peng J, Zhang N (2018) Differential expression of APE1 in hepatocellular carcinoma and the effects on proliferation and apoptosis of cancer cells. Biosci Trends 12(5):456–462. https://doi.org/10.5582/bst.2018.01239 Yang J, Yang D, Cogdell D, Du X, Li H, Pang Y, Sun Y, Hu L, Sun B, Trent J, Chen K, Zhang W (2010) APEX1 gene amplification and its protein overexpression in osteosarcoma: correlation with recurrence, metastasis, and survival. Technol Cancer Res Treat 9(2):161–169. https://doi.org/10.1177/153303461000900205 Ma Y, She XG, Ming YZ, Wan QQ (2014) miR-24 promotes the proliferation and invasion of HCC cells by targeting SOX7. Tumour Biol 35(11):10731–10736. https://doi.org/10.1007/s13277-014-2018-6 Zhang H, Duan J, Qu Y, Deng T, Liu R, Zhang L, Bai M, Li J, Ning T, Ge S, Wang X, Wang Z, Fan Q, Li H, Ying G, Huang D, Ba Y (2016) Onco-miR-24 regulates cell growth and apoptosis by targeting BCL2L11 in gastric cancer. Protein Cell 7(2):141–151. https://doi.org/10.1007/s13238-015-0234-5 Zhang S, Zhang C, Liu W, Zheng W, Zhang Y, Wang S, Huang D, Liu X, Bai Z (2015) MicroRNA-24 upregulation inhibits proliferation, metastasis and induces apoptosis in bladder cancer cells by targeting CARMA3. Int J Oncol 47(4):1351–1360. https://doi.org/10.3892/ijo.2015.3117 Zhu XF, Shan Z, Ma JY, Wang M, Zhang CX, Liu RM, Wu WB, Shi YW, Li W, Wang SM (2015) Investigating the role of the posttranscriptional gene regulator MiR-24- 3p in the proliferation, migration and apoptosis of human arterial smooth muscle cells in arteriosclerosis obliterans. Cell Physiol Biochem 36(4):1359–1370. https://doi.org/10.1159/000430302 Tong X, Wang X, Wang C, Li L (2018) Elevated levels of serum MiR-152 and miR-24 in uterine sarcoma: potential for inducing autophagy via SIRT1 and deacetylated LC3. Br J Biomed Sci 75(1):7–12. https://doi.org/10.1080/09674845.2017.1340225 Lang B, Shang C, Meng L (2016) Targeted Silencing of S100A8 Gene by miR-24 to Increase Chemotherapy Sensitivity of Endometrial Carcinoma Cells to Paclitaxel. Med Sci Monit 22:1953–1958. https://doi.org/10.12659/msm.899179 Funding Thanks for the support from the National Natural Science Foundation of China (Grant No. 81801421). Author information Authors and Affiliations Contributions ALT: protocol/project development; data collection or management; manuscript writing/editing. PR: data collection or management; data analysis; supervision. PXS: data analysis; manuscript writing/editing. Corresponding author Ethics declarations Conflict of interest The authors declare that they have no competing interests. Ethics approval All participants signed written informed consents and the protocol was approved by the Ethics Committees of the Wuhan University Renmin Hospital. Consent to participate All participants signed written informed consents and the protocol was approved by the Ethics Committees of the Wuhan University Renmin Hospital. Additional information Publisher's Note Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. This article has been retracted. Please see the retraction notice for more detail: https://doi.org/10.1007/s00404-026-08363-w Rights and permissions Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. About this article Cite this article Tan, A., Ruan, P. & Sun, P. RETRACTED ARTICLE: APEX1/miR-24 axis: a promising therapeutic target in endometriosis. Arch Gynecol Obstet 304, 131–141 (2021). https://doi.org/10.1007/s00404-021-05963-6 Received: Accepted: Published: Version of record: Issue date: DOI: https://doi.org/10.1007/s00404-021-05963-6

Text is read by the "Ask this paper" AI Q&A widget below. Extraction quality varies by source — PMC NXML preserves structure cleanly, OA-HTML may include some navigation residue, and OA-PDF can have broken hyphenation. The publisher copy (via DOI) is the canonical version.

My notes (saved in your browser only)

Ask this paper AI returns verbatim quotes from the full text · source: oa-doi-fallback

Answers must be backed by verbatim quotes from this paper's full text. Hallucinated quotes are dropped automatically; if no verbatim passage answers the question, we say so. How this works

Condition tags

endometriosis

MeSH descriptors

Cell Proliferation DNA-(Apurinic or Apyrimidinic Site) Lyase Endometriosis MicroRNAs MicroRNAs Apoptosis Cell Proliferation Cell Proliferation DNA-(Apurinic or Apyrimidinic Site) Lyase Endometrial Stromal Tumors Endometriosis Female Gene Expression Regulation Humans MicroRNAs Reverse Transcriptase Polymerase Chain Reaction

Citation neighborhood (no data yet)

We don't have any in-corpus citations linked to this paper yet. The paper's references may be in our DB but unresolved to ``paper_id`` (resolution happens at ingest when the cited DOI matches a row we already have). Run the cross-source citation reconcile pass to retry.

Source provenance

europepmc
last seen: 2026-08-03T06:10:56.557307+00:00
pubmed
last seen: 2026-05-13T22:24:55.077982+00:00
unpaywall
last seen: 2026-05-14T19:30:52.867331+00:00
License: public-domain-us · commercial use OK · attribution required
Courtesy of the U.S. National Library of Medicine