Evidence map›Paper›PMID 37483811›Full record

ArticleHeliyon2023

Knockdown of FUT11 inhibits the progression of gastric cancer via the PI3K/AKT pathway.

Wenpeng Cao, Zhirui Zeng, Jinzhi Lan, Yushi Yang, Min Lu, Shan Lei

Open access · goldAbstract read
In one paragraph

Article in Heliyon, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.7field-weighted citation impact, top 16% of its field
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

12 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Review
  6. Review
  7. Genomic analyses identify 15 risk loci and revealProceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  8. Article
  9. Article
  10. ProteinMolecules (Basel, Switzerland) · 2025
    Review
  11. Article
  12. 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

6 authors at 2 institutions in 1 country.

Wenpeng CaoDepartment of Anatomy, School of Basic Medicine, Guizhou Medical University, Guiyang 550009, Guizhou, China.
Zhirui ZengDepartment of Physiology, School of Basic Medicine, Guizhou Medical University, Guiyang 550009, Guizhou, China.
Jinzhi LanDepartment of Physiology, School of Basic Medicine, Guizhou Medical University, Guiyang 550009, Guizhou, China.
Yushi YangDepartment of Pathology, Affiliated Hospital of Guizhou Medical University, Guiyang 550009, Guizhou, China.
Min LuDepartment of Gastroenterology, Zhujiang Hospital, Southern Medical University, Guangzhou, 510000, Guangdong, China.
Shan LeiDepartment of Physiology, School of Basic Medicine, Guizhou Medical University, Guiyang 550009, Guizhou, China.
Guiyang Medical University · CNZhujiang Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gastric cancer (GC) is a common and highly malignant tumor of the digestive tract. Members of the focused fucosyltransferase (FUT) family participate in the advancement of various types of cancer. However, research of FUT family members in the progression of GC known to be limited. The purpose of the research was to determine the function of important affiliates of the FUT family in GC and to explore its impacts on the proliferation and migration of GC cells and molecular mechanisms. For the study, fucosyltransferase11 (FUT11) was confirmed to be the only affiliate of the FUT family that was upmodulated in GC tissues and linked to poor survival according to GEPIA data. Furthermore, compared with adjacent noncancerous tissues, the expression of FUT11 was increased in GC tissues. The elevated FUT11 expression suggested that the overall survival (OS) rate of GC is low. Inhibition of FUT11 significantly reduced the proliferation and migration and suppressed the PI3K/AKT pathway by down-regulated collagen type VI alpha 3 chain (COL6A3) in GC cells. The present study has demonstrated that reinstating the expression of COL6A3 in gastric cancer (GC) cells can counteract the inhibitory impact of FUT11 knockdown on the proliferation and migration of GC cells. In conclusion, FUT11 may serve as a novel biomarker for GC, as it modulates GC cell proliferation and migration through the PI3K/AKT signaling pathway.

Indexed as

COL6A3Fucosyltransferase familyFUT11Gastric cancerProliferation

Identifiers

PMID37483811
PMCPMC10362185
OpenAlexW4383500737

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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.