IntegratedProteomics Reveals Spliceosome Dysregulationand Highlights DHX9 as a TGF‑β Signaling-Driven FibrosisHub in Endometriosis

Mengjie Yang (403621), Lu Zhang (50563), Xinyu Ding (540853), Peitong Wei (21697130), Huaying Zhang (9157784), Jiahao Chen (194408), Yiqian Zhang (752795), Danyang Li (1490554), Zhengyi Chen (4386883), Dianchao Lin (6372341), Zhixiong Huang (3946337), Qionghua Chen (6372347)
2025 · doi:10.1021/acs.jproteome.5c00122.s002 · W7111346085
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Integrated proteomics of endometriosis samples identifies DHX9 as a TGF-β signaling-driven fibrosis hub, demonstrating that its downregulation attenuates lesion growth and collagen deposition in ectopic tissue.

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The provided text does not contain the body of a research paper but rather a standard browser cookie consent error message. It explains technical reasons why cookies might fail to set, such as browser settings or outdated system clocks, and describes how cookies are used for session management. Consequently, no scientific data, methods, or findings regarding biological mechanisms can be extracted from this input. The paper does not explicitly discuss endometriosis or adenomyosis; it was included in the corpus via a keyword match in the upstream search index.

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Abstract

Endometriosis (EM) is a chronic, estrogen-dependent disease characterized by the ectopic presence of endometrial-like tissue. Despite extensive research, its molecular pathogenesis remains unclear. In this study, we conducted an integrated proteomic network analysis using 22 endometrial samples to investigate protein-level alterations in ectopic lesions. Using weighted protein coexpression network analysis (WGCNA), we identified 12 protein modules strongly associated with EM clinical traits, with the turquoise module exhibiting significant downregulation of spliceosome-related proteins in ectopic tissues. Within this module, DHX9 emerged as a top hub protein, validated as significantly downregulated in ectopic (EC) tissues at both mRNA and protein levels. Functional studies demonstrated that DHX9 knockdown in endometrial stromal cells (ESCs) inhibited proliferation and, crucially, attenuated fibrogenesis. Proteomic profiling revealed that DHX9 knockdown downregulated proteins involved in the TGF-β signaling pathway and extracellular matrix organization. Consistent with this, DHX9 knockdown in a mouse endometriosis model significantly reduced ectopic lesion growth and collagen deposition. These findings establish DHX9 as a key regulator, promoting ESC fibrogenesis via TGF-β signaling, and implicate spliceosomal dysfunction in EM pathogenesis, highlighting DHX9 as a potential therapeutic target.
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last seen: 2026-06-04T00:00:01.174412+00:00
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