DLK1/IGF-2 Axis Promotes the Migration and Adhesion of Ectopic Endometrial Stromal Cells in Endometriosis

Lili Dong, Gaiwen Liu, Huiying Xiao
In: JOURNAL OF BIOLOGICAL REGULATORS AND HOMEOSTATIC AGENTS · 2023 · vol. 37(10) · doi:10.23812/j.biol.regul.homeost.agents.20233710.518 · W4407306473
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DLK1 silencing in ectopic endometrial stromal cells reduces viability, migration, and adhesion by downregulating IGF-2, thereby suppressing lesion growth in an endometriosis mouse model.

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This study investigated the role of the DLK1/IGF-2 axis in the pathogenesis of endometriosis by analyzing expression levels in normal and ectopic endometrial tissues. The researchers found that DLK1 and IGF-2 were highly expressed in ectopic endometrial stromal cells, where DLK1 positively regulated IGF-2 to promote cell viability, migration, and adhesion. Experimental silencing of DLK1 inhibited these cellular behaviors and reduced lesion size and weight in an endometriosis mouse model. This paper is centrally about endometriosis — specifically focusing on the molecular mechanisms driving ectopic endometrial stromal cell behavior.

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Abstract

Background: Endometriosis affects 5%–10% of fertile women globally. Microarray analysis predicted that Delta-like non-canonical Notch ligand 1 (DLK1) is differentially expressed in normal endometrium tissues (NET) and ectopic endometrial tissues (EET). Insulin-like growth factor 2 (IGF-2) is closely associated with endometriosis. This study aimed to clarify whether the DLK1/IGF-2 axis is involved in the pathogenesis of endometriosis. Methods: DLK1 and IGF-2 expression in endometrial tissues and endometrial stromal cells were measured by quantitative real-time polymerase chain reaction, western blotting, and immunohistochemical assays. After knockdown DLK1 in ectopic endometrial stromal cells (EESCs), cellular behaviors were evaluated using cell counting kit-8, transwell assay, wound healing assay, and western blotting. The interaction between DLK1 and IGF-2 was verified using luciferase reporter assay and RNA-binding protein immunoprecipitation. Finally, an endometriosis mouse model was generated to evaluate the effect of DLK1 on lesion. Results: DLK1 was highly expressed in EET and EESCs. DLK1 silencing inhibited EESC viability, migration, and adhesion. Moreover, IGF-2, which can interact with and is positively regulated by DLK1, was highly expressed in EET and EESCs. IGF-2 overexpression abrogated the biological function of EESCs induced by DLK1 depletion. In addition, DLK1 knockdown suppressed endometrial lesion size and weight and attenuated histopathology. Conclusions: Silencing the DLK1/IGF-2 axis attenuates endometriosis progression by inhibiting EESC viability, migration, and adhesion. These results indicated that the DLK1/IGF-2 axis may be a therapeutic target for the treatment of endometriosis.
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Abstract

Background: Endometriosis affects 5%–10% of fertile women globally. Microarray analysis predicted that Delta-like non-canonical Notch ligand 1 (DLK1) is differentially expressed in normal endometrium tissues (NET) and ectopic endometrial tissues (EET). Insulin-like growth factor 2 (IGF-2) is closely associated with endometriosis. This study aimed to clarify whether the DLK1/IGF-2 axis is involved in the pathogenesis of endometriosis. Methods: DLK1 and IGF-2 expression in endometrial tissues and endometrial stromal cells were measured by quantitative real-time polymerase chain reaction, western blotting, and immunohistochemical assays. After knockdown DLK1 in ectopic endometrial stromal cells (EESCs), cellular behaviors were evaluated using cell counting kit-8, transwell assay, wound healing assay, and western blotting. The interaction between DLK1 and IGF-2 was verified using luciferase reporter assay and RNA-binding protein immunoprecipitation. Finally, an endometriosis mouse model was generated to evaluate the effect of DLK1 on lesion. Results: DLK1 was highly expressed in EET and EESCs. DLK1 silencing inhibited EESC viability, migration, and adhesion. Moreover, IGF-2, which can interact with and is positively regulated by DLK1, was highly expressed in EET and EESCs. IGF-2 overexpression abrogated the biological function of EESCs induced by DLK1 depletion. In addition, DLK1 knockdown suppressed endometrial lesion size and weight and attenuated histopathology. Conclusions: Silencing the DLK1/IGF-2 axis attenuates endometriosis progression by inhibiting EESC viability, migration, and adhesion. These results indicated that the DLK1/IGF-2 axis may be a therapeutic target for the treatment of endometriosis.

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References Supporting Agencies Copyright (c) 2023 Lili Dong, Gaiwen Liu, Huiying Xiao This site is licensed under a Creative Commons Attribution 4.0 International License (CC BY 4.0). Medical Genetics, University of Torino Medical School, Italy Department of Biomedical, Surgical and Dental Sciences, University of Milan, Italy

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