ArticleCancer gene therapy2026
COL3A1 promotes gastric cancer progression by activating PI3K/AKT signaling.
Article in Cancer gene therapy, 2026. 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
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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.
- Macrophage-derived CTSZ promotes prostate cancer progression via αVβ3 integrin-mediated activation of the AKT/FOXO1/JUNB signaling axis.Cancer cell international · 2026Article
- MUC16 promotes endometrial cancer progression and modulates sensitivity to lapatinib through the ESR1/PI3K/AKT axis.Translational oncology · 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
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
COL3A1 plays an oncogenic role in several types of cancer; however, the function of COL3A1 in gastric cancer (GC) remains unknown. The present study investigated the function and possible molecular mechanisms of COL3A1 in GC. The results showed that COL3A1 mRNA and protein were overexpressed in GC tissues and cells, and is associated with Immune microenvironment remodeling. High COL3A1 expression indicates poor prognosis. ESR1 transcriptionally elevates COL3A1 expression in GC. COL3A1-integrin α1 autocrine and paracrine axis promotes the proliferation, invasion, and angiogenesis of GC by activating PI3K-AKT signaling pathway. Targeting COL3A1 could significantly inhibit GC growth in vivo. Collectively, our findings indicated that COL3A1 could act as an oncogene in GC through regulating the PI3K-AKT signaling pathway.
Indexed as
Identifiers
41723290What 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.