LINC01541 Functions as a ceRNA to Modulate the Wnt/β-Catenin Pathway by Decoying miR-506-5p in Endometriosis

article OA: closed CC0 ⤵ 12 in-corpus citations
AI-generated summary by claude@2026-06+body, 2026-06-07

In endometriosis, LINC01541 sponges miR-506-5p, relieving inhibition of WIF1 and thus activating the Wnt/β-catenin pathway.

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

AI-generated deep summary by claude@2026-06, 2026-06-07 · read from full text

This study investigated how the long noncoding RNA LINC01541 regulates the Wnt/β-catenin pathway in endometriosis by functioning as a competing endogenous RNA that decoys miR-506-5p. Using tissue samples from healthy controls and patients with endometriosis (n=10 and n=18) and mechanistic experiments in 17β-estradiol-stimulated endometrial stromal cells, the authors found that LINC01541 was decreased while miR-506-5p was increased in ectopic lesions, with a negative correlation between them. They reported that miR-506-5p activated Wnt/β-catenin signaling by inhibiting WIF1 expression, promoting ESC proliferation, migration, and invasion, while miR-506-5p silencing increased apoptosis and suppressed proliferation; importantly, miR-506-5p overexpression reversed LINC01541’s inhibitory effects in this model. The paper’s limitation is that its functional evidence is based on in vitro ESC experiments rather than in vivo confirmation. This paper is centrally about endometriosis—LINC01541 regulating the Wnt/β-catenin pathway via miR-506-5p to modulate endometrial stromal cell behaviors.

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

Full text 8,688 characters · extracted from oa-doi-fallback · 2 sections · click to expand

Abstract

Endometriosis is one of the most common gynecological diseases that adversely effects the lives of women. Our previous studies showed that LINC01541 plays a key role in 17β-estradiol (17β-E2)-stimulated endometrial stromal cells (ESCs); however, the mechanism by which LINC01541 exerts if effects requires further elaboration. Here, we report that LINC01541 serves to reduce the bioavailability of miR-506-5p by acting as a molecular sponge. Samples of control endometrial tissue and ectopic endometrial tissue were obtained from 10 healthy volunteers and 18 patients with endometriosis, respectively, and the levels of LINC01541 and miR-506-5p expressions in those tissues were measured. The relationship between LINC01541 and miR-506-5p was verified in 17β-E2-stimulated ESCs. Overexpression or silencing of miR-506-5p in ESCs was performed explore its role in endometriosis, and we also investigated whether WNT inhibitory factor 1 (WIF1) might be a target gene of miR-506-5p. Our results showed that LINC01541 was expressed at low levels and miR-506-5p was expressed at high levels in ectopic tissues. LINC01541 expression was negatively correlated with miR-506-5p expression. We also found that miR-506-5p activated the Wnt/β-catenin pathway by inhibiting WIF1 expression, and thereby induced the proliferation, migration, and invasion of ESCs. Furthermore, silencing of miR-506-5p promoted apoptosis and suppressed the proliferation of 17β-E2-treated ESCs. Overexpression of miR-506-5p could reverse the inhibitory effect of LINC01541 in endometriosis. In summary, this study found that in endometriosis, LINC01541 functions as a ceRNA that modulates the Wnt/β-catenin pathway by decoying miR-506-5p. Similar content being viewed by others

References

Andrade SS, Azevedo ADC, Monasterio ICG, Paredes-Gamero EJ, Gonçalves GA, Bonetti TC, et al. 17β-Estradiol and steady-state concentrations of H2O2: antiapoptotic effect in endometrial cells from patients with endometriosis. Free Radical Biology Medicine. 2013;60:63–72. Cai W, Xu Y, Yin J, Zuo W, Su Z. miR-552-5p facilitates osteosarcoma cell proliferation and metastasis by targeting WIF1. Exp Ther Med. 2019;17:3781–8. Delvoux B, Groothuis P, D’Hooghe T, Kyama C, Dunselman G, Romano A. Increased production of 17beta-estradiol in endometriosis lesions is the result of impaired metabolism. J Clin Endocrinol Metab. 2009;94:876–83. Dunselman GAJ, Vermeulen N, Becker C, et al. ESHRE guideline: management of women with endometriosis. Hum Reprod. 2014;29:400–12. Ghazal S, Mckinnon B, Zhou J, et al. H19 lncRNA alters stromal cell growth via IGF signaling in the endometrium of women with endometriosis. Embo Molecular Medicine. 2015;7:996–1003. Giudice LC, Kao LC. Endometriosis. Lancet. 2004;364:1789–99. Guo M, Zhang X, Wang G, Sun J, Jiang Z, Khadarian K, et al. miR-603 promotes glioma cell growth via Wnt/beta-catenin pathway by inhibiting WIF1 and CTNNBIP1. Cancer Lett. 2015;360:76–86. Hui Z, Zhao X, Shu L, et al. 17βE 2 promotes cell proliferation in endometriosis by decreasing PTEN via NFκB-dependent pathway. Molecular Cellular Endocrinology. 2010;317:31–43. Ilangavan K, Kalu E. High prevalence of endometriosis in infertile women with normal ovulation and normospermic partners. Fertility & Sterility. 2009;92:68–74. Janssen EB, Rijkers AC, Hoppenbrouwers K, et al. Prevalence of endometriosis diagnosed by laparoscopy in adolescents with dysmenorrhea or chronic pelvic pain: a systematic review. Hum Reprod Update. 2013;19:570–82. Jun D, Wan L, Xiaojun X, et al. MicroRNA-506 inhibits gastric cancer proliferation and invasion by directly targeting Yap1. Tumour Biol. 2015;36:6823–31. Kapranov P, Cheng J, Dike S, Nix DA, Duttagupta R, Willingham AT, et al. RNA maps reveal new RNA classes and a possible function for pervasive transcription. Science. 2007;316:1484–8. Khan KN, Kitajima M, Inoue T, Fujishita A, Nakashima M, Masuzaki H. 17β-estradiol and lipopolysaccharide additively promote pelvic inflammation and growth of endometriosis. Reprod Sci. 2015;22:585–94. Li C, Wang Z, Chen S, et al. MicroRNA-552 promotes hepatocellular carcinoma progression by downregulating WIF1. Int J Mol Med. 2018;42:3309–17. Liang J, Chen C, Liu H, et al. Gossypol promotes Wnt/beta-catenin signaling through WIF1 in ovariectomy-induced osteoporosis. Biomed Res Int. 2019;2019:8745487. Lingbao A, Qian T, Sheng Z, et al. Inactivation of Wnt inhibitory factor-1 (WIF1) expression by epigenetic silencing is a common event in breast cancer. Carcinogenesis. 2006;27:1341–8. Maged AM, Deeb WS, Amir AE, et al. Diagnostic accuracy of serum miR-122 and miR-199a in women with endometriosis. Int J Gynaecol Obstet. 2017;141:14–9. Mai H, Wei Y, Yin Y, Huang S, Lin H, Liao Y, et al. LINC01541 overexpression attenuates the 17beta-estradiol-induced migration and invasion capabilities of endometrial stromal cells. Syst Biol Reprod Med. 2019;65:214–22. Okamoto M, Nasu K, Abe W, Aoyagi Y, Kawano Y, Kai K, et al. Enhanced miR-210 expression promotes the pathogenesis of endometriosis through activation of signal transducer and activator of transcription 3. Hum Reprod. 2015;30:632–41. Pateisky P, Pils D, Szabo L, Kuessel L, Husslein H, Schmitz A, et al. hsa-miRNA-154-5p expression in plasma of endometriosis patients is a potential diagnostic marker for the disease. Reprod BioMed Online. 2018;37:449–66. Pei L, Shen JK, Hornicek FJ, et al. Wnt inhibitory factor 1 (WIF1) methylation and its association with clinical prognosis in patients with chondrosarcoma. Sci Rep. 2017;7:1580. Ramachandran I, Thavathiru E, Ramalingam S, Natarajan G, Mills WK, Benbrook DM, et al. Wnt inhibitory factor 1 induces apoptosis and inhibits cervical cancer growth, invasion and angiogenesis in vivo. Oncogene. 2012;31:2725–37. Rong W, Zhai Y, Leung JY, et al. WIF-1 is a downstream target of β-catenin/TCF and acts as a negative feedback regulator of Wnt signaling. Cancer Research. 2004;64:1112. Ruixi L, Ruobai S, Hicks GR, et al. Arabidopsis ribosomal proteins control vacuole trafficking and developmental programs through the regulation of lipid metabolism. PNAS. 2014;2014:89–98. Sha L, Huang L, Luo X, Bao J, Gao L, Pan Q, et al. Long non-coding RNA LINC00261 inhibits cell growth and migration in endometriosis. Journal of Obstetrics Gynaecology Research. 2017;43:1563–9. Simoens S, Dunselman G, Dirksen C, Hummelshoj L, Bokor A, Brandes I, et al. The burden of endometriosis: costs and quality of life of women with endometriosis and treated in referral centres. Hum Reprod. 2012;27:1292–9. Stock M, Böhm C, Scholtysek C, Englbrecht M, Fürnrohr BG, Klinger P, et al. Wnt inhibitory factor 1 deficiency uncouples cartilage and bone destruction in tumor necrosis factor α–mediated experimental arthritis. Arthritis Rheumatism. 2013;65:2310–22. Sun PR, Jia SZ, Lin H, Leng JH, Lang JH. Genome-wide profiling of long noncoding ribonucleic acid expression patterns in ovarian endometriosis by microarray. Fertility & Sterility. 2014;101:1038–46. Sun H, Wang G, Peng Y, et al. H19 lncRNA mediates 17beta-estradiol-induced cell proliferation in MCF-7 breast cancer cells. Oncol Rep. 2015;33:3045–52. Taylor DH, Chu ET, Spektor R, et al. Long non-coding RNA regulation of reproduction and development. Molecular Reproduction Development. 2016;82:932–56. Wang WT, Sun YM, Huang W, He B, Zhao YN, Chen YQ. Genome-wide long non-coding RNA analysis identified circulating LncRNAs as novel non-invasive diagnostic biomarkers for gynecological disease. Sci Rep. 2016;6:23343. Zhang H, Hu B, Wang Z, et al. miR-181c contributes to cisplatin resistance in non-small cell lung cancer cells by targeting Wnt inhibition factor 1. Cancer Chemotherapy Pharmacology. 2017;80:1–12. Author information Authors and Affiliations Corresponding author Ethics declarations All procedures involving human participants were performed in accordance with ethical standards of the institutional and/or national research committee, as well as with the 1964 Helsinki Declaration and its later amendments or comparable ethical standards. Conflict of Interest All authors declare that they have no conflict of interest. Additional information Publisher’s Note Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. Rights and permissions About this article Cite this article Mai, H., Xu, H., Lin, H. et al. LINC01541 Functions as a ceRNA to Modulate the Wnt/β-Catenin Pathway by Decoying miR-506-5p in Endometriosis. Reprod. Sci. 28, 665–674 (2021). https://doi.org/10.1007/s43032-020-00295-3 Received: Accepted: Published: Version of record: Issue date: DOI: https://doi.org/10.1007/s43032-020-00295-3

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

mesh:D004715endometriosis

MeSH descriptors

Adaptor Proteins, Signal Transducing Endometriosis Endometrium MicroRNAs RNA, Long Noncoding Stromal Cells Wnt Signaling Pathway Adaptor Proteins, Signal Transducing Adaptor Proteins, Signal Transducing Adult Case-Control Studies Cell Movement Cell Proliferation Cells, Cultured Endometriosis Endometriosis Endometriosis Endometrium Endometrium Endometrium

Citation neighborhood

Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. [ expand to 2 hops ] — adds papers reached through this work's immediate citers/citees. Heavier; up to 60 extra dots.

References (37)

Cited by (12)

Source provenance

europepmc
last seen: 2026-06-04T01:30:01.192114+00:00
openalex
last seen: 2026-06-04T00:00:01.174412+00:00
pubmed
last seen: 2026-05-13T22:21:47.975235+00:00
unpaywall
last seen: 2026-06-02T02:00:03.124865+00:00
License: CC0 · commercial use OK