IGF2BP1 promotes endometriosis by enhancing m6A modification stability of HMGB1

Xin Wei, Su Y, Yanlin Su, Tian W, Wencai Tian, Cheng L, Cheng Li, Li Cheng, Ling Yin, Yin L, Xiaoxia He, He X
Journal of Obstetrics and Gynaecology Research · 2025 · vol. 51(2) , pp. e16242 · doi:10.1111/jog.16242 · PMID:39967010 · W4407758222
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IGF2BP1 promotes endometriosis by binding to HMGB1 mRNA and stabilizing it through m6A modification, thereby enhancing cell proliferation, migration, and invasion.

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This study investigated the role of IGF2BP1 and HMGB1 in endometriosis by analyzing their expression levels in normal, eutopic, and ectopic endometrial tissues. The researchers found that both proteins were elevated in ectopic tissue and positively correlated, with IGF2BP1 binding to HMGB1 mRNA to enhance its stability through m6A modification. In vitro and in vivo experiments demonstrated that inhibiting IGF2BP1 reduced cell proliferation, invasion, and lesion size, while overexpressing HMGB1 reversed these effects. This paper is centrally about endometriosis — specifically elucidating a molecular mechanism involving m6A modification and protein stability in disease progression.

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Abstract

BACKGROUND: Endometriosis is a chronic inflammatory condition afflicting women of reproductive age. Our study aims to clarify the function and mechanism of insulin-like growth factor 2 mRNA-binding protein 1 (IGF2BP1) and high mobility group box 1 protein (HMGB1) in endometriosis. METHODS: HMGB1 and various N6-methyladenosine (m6A) reader protein levels were assessed in normal, eutopic, and ectopic endometrial tissue, and a correlation analysis was conducted. The impact of IGF2BP1 knockdown on endometriosis was assessed both in vivo in rat models and in vitro in ectopic endometrial stromal cells (eESCs) using methods such as immunoblotting and mRNA quantification. The binding of IGF2BP1 to HMGB1 mRNA in eESCs was assessed using RIP-PCR. Following transfection with sh-IGF2BP1 and oe-HMGB1, the expression of IGF2BP1 and HMGB1, as well as cell proliferation, invasion, and migration abilities, were measured in eESCs. RESULTS: In ectopic endometrial tissue, IGF2BP1 and HMGB1 were elevated and positively correlated. Inhibition of IGF2BP1 reduced eESC proliferation, migration, invasion, and glucose intake. Meanwhile, HMGB1, PKM2, and HK2 expression were depressed. In vivo, results were consistent with in vitro. Additionally, in vivo experiments confirmed that inhibition of IGF2BP1 resulted in reduced ectopic endometrial lesion spherical volume, weight, and interstitial lesions. IGF2BP1 bound to HMGB1 mRNA and enhanced its stability by m6A modification. Conversely, when IGF2BP1 was knocked down and HMGB1 was overexpressed, the results were opposite to those observed previously. CONCLUSION: IGF2BP1 promotes endometriosis progression by enhancing m6A modification stability of HMGB1. This study provides a theoretical basis for identifying therapeutic targets for endometriosis.
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Abstract

Background Endometriosis is a chronic inflammatory condition afflicting women of reproductive age. Our study aims to clarify the function and mechanism of insulin-like growth factor 2 mRNA-binding protein 1 (IGF2BP1) and high mobility group box 1 protein (HMGB1) in endometriosis.

Methods

HMGB1 and various N6-methyladenosine (m6A) reader protein levels were assessed in normal, eutopic, and ectopic endometrial tissue, and a correlation analysis was conducted. The impact of IGF2BP1 knockdown on endometriosis was assessed both in vivo in rat models and in vitro in ectopic endometrial stromal cells (eESCs) using methods such as immunoblotting and mRNA quantification. The binding of IGF2BP1 to HMGB1 mRNA in eESCs was assessed using RIP-PCR. Following transfection with sh-IGF2BP1 and oe-HMGB1, the expression of IGF2BP1 and HMGB1, as well as cell proliferation, invasion, and migration abilities, were measured in eESCs.

Results

In ectopic endometrial tissue, IGF2BP1 and HMGB1 were elevated and positively correlated. Inhibition of IGF2BP1 reduced eESC proliferation, migration, invasion, and glucose intake. Meanwhile, HMGB1, PKM2, and HK2 expression were depressed. In vivo, results were consistent with in vitro. Additionally, in vivo experiments confirmed that inhibition of IGF2BP1 resulted in reduced ectopic endometrial lesion spherical volume, weight, and interstitial lesions. IGF2BP1 bound to HMGB1 mRNA and enhanced its stability by m6A modification. Conversely, when IGF2BP1 was knocked down and HMGB1 was overexpressed, the results were opposite to those observed previously.

Conclusion

IGF2BP1 promotes endometriosis progression by enhancing m6A modification stability of HMGB1. This study provides a theoretical basis for identifying therapeutic targets for endometriosis. CONFLICT OF INTEREST STATEMENT The authors declare that this article has no conflicts of interest. DATA AVAILABILITY STATEMENT All data found during this study are included in the article or available from the authors.

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Condition tags

endometriosis

MeSH descriptors

Adenosine Adenosine Adenosine Adenosine Adenosine Adenosine Adenosine Adenosine Adenosine Adenosine Adenosine Adenosine Adenosine Adenosine Adenosine Adenosine Adenosine Adenosine Adenosine Adenosine

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.

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