Evidence map›Paper›PMID 37929733›Full record

ArticleCurrent gene therapy2024

FIGNL1 Promotes Hepatocellular Carcinoma Formation

Jiabei Wang, Linmao Sun, Yao Liu, Yunguang Zhang

Open access · hybridAbstract read
In one paragraph

Article in Current gene therapy, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

29 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Identification ofEndocrine, metabolic & immune disorders drug targets · 2026
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

4 authors at 1 institution in 1 country.

Jiabei WangAnhui Province Key Laboratory of Hepatopancreatobiliary Surgery, Department of Hepatobiliary Surgery, Division of Life Sciences and Medicine, The First Affiliated Hospital of USTC, University of Science and Technology of China, Hefei, 230001, China.
Linmao SunAnhui Province Key Laboratory of Hepatopancreatobiliary Surgery, Department of Hepatobiliary Surgery, Division of Life Sciences and Medicine, The First Affiliated Hospital of USTC, University of Science and Technology of China, Hefei, 230001, China.
Yao LiuAnhui Province Key Laboratory of Hepatopancreatobiliary Surgery, Department of Hepatobiliary Surgery, Division of Life Sciences and Medicine, The First Affiliated Hospital of USTC, University of Science and Technology of China, Hefei, 230001, China.
Yunguang ZhangAnhui Province Key Laboratory of Hepatopancreatobiliary Surgery, Department of Hepatobiliary Surgery, Division of Life Sciences and Medicine, The First Affiliated Hospital of USTC, University of Science and Technology of China, Hefei, 230001, China.
University of Science and Technology of China · CN

Funding

National Natural Science Foundation of China 82272787Natural Science Foundation of Anhui Province 2008085QH376
6 · The paper itself

Abstract

backgroundThe development of novel biomarkers is crucial for the treatment of HCC. In this study, we investigated a new molecular therapeutic target for HCC. Fidgetin-like 1 (FIGNL1) has been reported to play a vital role in lung adenocarcinoma. However, the potential function of FIGNL1 in HCC is still unknown.

objectiveThis study aims to investigate the key regulatory mechanisms of FIGNL1 in the formation of HCC.

methodsThe regulatory effect of FIGNL1 on HCC was studied by lentivirus infection.

resultsFunctionally, we demonstrated that FIGNL1 knockdown significantly inhibited HCC cell proliferation, migration and promoted cell apoptosis

conclusionOur study revealed that FIGNL1 could modulate the ECM-receptor interaction pathway through the regulation of HMMR, thus regulating the formation of HCC.

Indexed as

ApoptosisATPases Associated with Diverse Cellular ActivitiesCarcinoma, HepatocellularCell MovementCell ProliferationLiver NeoplasmsMembrane ProteinsMicrotubule-Associated ProteinsNuclear ProteinsAnimalsCell Line, TumorExtracellular MatrixGene Expression Regulation, NeoplasticHumansMiceMice, NudeATPases Associated with Diverse Cellular ActivitiesFIGNL1 protein, humanMembrane ProteinsMicrotubule-Associated ProteinsNuclear ProteinsRNA Splicing FactorsTM4SF5 protein, humanextracellular matrix-receptor interaction pathwayfidgetin-like 1Hepatocellular carcinomahyaluronan mediated motility receptornovel targetsystematic treatment

Identifiers

PMID37929733
PMCPMC11071652
OpenAlexW4388421421

What OpenQuestion holds

Textmetadata
LicenceCC BY
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 OpenQuestion graph.