Evidence map›Paper›PMID 41723290›Full record

ArticleCancer gene therapy2026

COL3A1 promotes gastric cancer progression by activating PI3K/AKT signaling.

Xiaqiong Mao, Wei Li, Yue Guan, Xiaoyi Kuai, Jie Yuan

Abstract read
PubMed Publisher
In one paragraph

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.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Article
  2. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors.

Xiaqiong Mao *Department of Gastroenterology, Nanjing First Hospital, Nanjing Medical University, Nanjing, Jiangsu, China.
Wei Li *Department of Gastroenterology, Fourth People's Hospital of Taizhou, Taizhou, China.
Yue Guan *Department of Gastroenterology, Nanjing First Hospital, Nanjing Medical University, Nanjing, Jiangsu, China.
Xiaoyi KuaiDepartment of Gastroenterology, The Affiliated Suzhou Hospital of Nanjing Medical University, Suzhou, Jiangsu, China. zoekxy@126.com.ORCID http://orcid.org/0000-0002-0788-9178
Jie YuanDepartment of Gastroenterology, Nanjing First Hospital, Nanjing Medical University, Nanjing, Jiangsu, China. jim0790@sina.com.ORCID http://orcid.org/0009-0002-7172-0729

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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

Collagen Type IIISignal TransductionStomach NeoplasmsAnimalsCell Line, TumorCell ProliferationDisease ProgressionEstrogen Receptor alphaFemaleGene Knockdown TechniquesHeterograftsHumansIntegrin alpha1MiceMice, Inbred BALB CNeoplasm InvasivenessCOL3A1 protein, humanCollagen Type IIIESR1 protein, humanEstrogen Receptor alphaIntegrin alpha1

Identifiers

What Socratic holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.