ArticleRespiratory research2026
Integrated multi-omics analysis reveals GPD1L-mediated dysregulation of glycerophospholipid metabolism facilitates the progression of lung adenocarcinoma.
Article in Respiratory research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
Abstract
backgroundWith the widespread of low-dose computed tomography (LDCT), an increasing number of early-stage lung adenocarcinomas (LUAD) presenting as ground-glass opacity (GGO) nodules are being detected. However, the metabolic dysregulation involved in the progression from GGO to solid nodule remains poorly understood. In this study, we investigated the significance of GPD1L-mediated glycerophospholipid metabolism dysregulation during this transition and explored potential therapeutic targets.
methodsWe conducted analysis on multi-omics of lung adenocarcinoma, including bulk RNA-seq, whole-exome sequencing, metabolomics and single-cell RNA seq data. Extensive experiments were conducted to validate the role of GPD1L and the potential therapeutic target GPX4. Rescue assays were performed to further elucidate the mechanism.
resultsMulti-omics analysis revealed the essential role of GPD1L-mediated glycerophospholipid metabolism dysregulation between ground-glass opacity and solid nodule. Knockdown of GPD1L in lung adenocarcinoma cell lines promoted tumor progression and attenuated the degradation of HIF-1α, conferring resistance to hypoxia and apoptosis. Metabolomics, transcriptomics, and in vitro experiments further demonstrated that GPD1L downregulation impairs GPX4 expression by reducing AKT phosphorylation. In addition, GPD1L expression was associated with poor prognosis and may serve as a potential biomarker for immunotherapy.
conclusionGPD1L-mediated glycerophospholipid metabolism dysregulation promotes lung adenocarcinoma progress by stabilizing HIF- 1α. Meanwhile, GPX4 were downregulates via AKT/NRF2/GPX4 pathway, suggesting a potential therapeutic target.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.