ArticleDiscover oncology2025
Syndecan-4 promotes gastric cancer progression through activating TGF-β1 induced lipid reprogramming and contributes positive loop circuits.
Article in Discover oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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
2 citing papers in PubMed.
- The role of ECM mechanics in cancer mechanotransduction through unraveling the molecular machinery of integrins, FAK, and YAP signaling.Cellular & molecular biology letters · 2026Review
- GPNMB-ECD drives acquired resistance to osimertinib in NSCLC via inducing tumor cell cytoskeletal reorganization.Cellular & molecular biology letters · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
backgroundSyndecan-4 (SDC4) plays a pivotal role in tumorigenesis through cell signaling, adhesion and matrix interactions. Lipid reprogramming is a core strategy for malignant tumors to drive progression and invasion through reshaping immunity, stromal and vascular ecology in microenvironment. However, the regulatory mechanism of SDC4 in lipid reprogramming has not yet been elucidated. Therefore, it is important to investigate underlying mechanisms and develop novel therapeutic targets for gastric cancer (GC).
methodsClinicopathological data and corresponding immunohistochemistry were collected to explore the role of SDC4 in patients with GC. Functional experiments were performed to assess tumor progression and lipid reprogramming. Moreover, western blot assay was performed to verify the molecular mechanisms. In addition, cholesterol-induced lipotoxic environments both in vivo and in vitro were constructed to explore the underlying positive loop circuit.
resultsSDC4 expression was upregulated in tumor tissues compared to normal gastric tissues and was associated with differentiation grades. Patients with high SDC4 expression were positively correlated with high circulating tumor cell (CTC) levels, vascular endothelial growth factor (VEGF) levels and poor prognosis. Moreover, SDC4 significantly promoted tumor progression by activating transforming growth factor-beta 1 (TGF-β1/TGFB1)-induced lipid reprogramming and contributed a positive loop circuit in GC cells. However, the core of this circuit was dependent on Smad3. In addition, a cholesterol-induced lipotoxic environment upregulated SDC4 expression by activating the RAS signaling pathway and further indicated a positive loop circuit between SDC4 and lipid reprogramming in GC.
conclusionsThese findings highlight SDC4 as a therapeutic target for GC and identify actionable positive loop circuits.
Indexed as
Identifiers
What Socratic 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 Socratic graph.