ArticleBiology direct2025
HMGA1 promotes the progression of lung adenocarcinoma through the STAT1-mediated transcriptional activation of DDAH1.
Article in Biology direct, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Identifying Epithelial-Cell Progression Signatures (ECPSs) from Multi-Resolution Multi-Omics Data for Translational Clinical Applications in Lung Adenocarcinoma.International journal of molecular sciences · 2026Article
- E2F-mediated activation of mTORC1 through the ubiquitin-proteasome system promotes lung adenocarcinoma progression.Cell death & disease · 2026Article
- [Integrative Analysis of Multi-source Public Databases to Screen Core Genes for Constructing A Prognostic Risk Model in Lung Adenocarcinoma].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2025Article
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Authors and funding
7 authors.
Funding
Abstract
backgroundAdvancements in precision oncology have generated increased interest in the prognostic and therapeutic capabilities of transcription factors, among which HMGA1 is significantly correlated with LUAD prognosis. However, our understanding of HMGA1 remains insufficient. This study seeks to elucidate the biological functions of HMGA1 and to investigate the underlying mechanisms.
methodsThe prognostic value of HMGA1 was validated across multiple independent patient cohorts with LUAD, and its impact on tumor proliferation was verified by both in vitro and in vivo models. A series of experiments were performed to investigate the underlying molecular mechanism, including RNA sequencing, co-immunoprecipitation and chromatin immunoprecipitation.
resultsHMGA1 plays a crucial role in promoting the proliferation of LUAD. The underlying mechanism involves the recruitment of STAT1 to the promoter region of DDAH1, which synergistically increases its transcription and subsequently activates the ADMA/NO signaling pathway. Notably, the STAT1 inhibitor fludarabine has been shown to effectively impede the progression of LUAD models characterized by high levels of HMGA1.
conclusionOur research reveals a previously unrecognized mechanism through which the HMGA1/STAT1 complex facilitates LUAD proliferation by transcriptionally activating DDAH1. Moreover, we propose that fludarabine could serve as a promising therapeutic option for LUAD patients exhibiting elevated levels of HMGA1.
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