Evidence map›Paper›PMID 31876386›Full record

ArticleJournal of cellular and molecular medicine2021

TM4SF1, a binding protein of DVL2 in hepatocellular carcinoma, positively regulates beta-catenin/TCF signalling.

ChuanrRong Zhu, XiaoLing Luo, JinSheng Wu, YuTing Liu, Lei Liu, ShiJie Ma, Rui Xie, ShaoChuang Wang, Wu Ji

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
0.9field-weighted citation impact, top 25% 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

17 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
  2. YBX1 Enhances the Stability of TM4SF1 in an mCombinatorial chemistry & high throughput screening · 2026
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  16. Recent progress in treatment of hepatocellular carcinoma.American journal of cancer research · 2020
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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

9 authors at 2 institutions in 1 country.

ChuanrRong ZhuDepartment of General Surgery, Jinling Clinical Medical College, Nanjing Medical University, Nanjing, China.
XiaoLing LuoDepartment of Gastroenterology, The Affiliated Huai'an No.1 People's Hospital of Nanjing Medical University, Huai'an, China.
JinSheng WuDepartment of Hepatobiliary & Pancreatic Surgery, The Affiliated Huai'an No.1 People's Hospital of Nanjing Medical University, Huai'an, China.
YuTing LiuDepartment of Hepatobiliary & Pancreatic Surgery, The Affiliated Huai'an No.1 People's Hospital of Nanjing Medical University, Huai'an, China.
Lei LiuDepartment of Hepatobiliary & Pancreatic Surgery, The Affiliated Huai'an No.1 People's Hospital of Nanjing Medical University, Huai'an, China.
ShiJie MaDepartment of Gastroenterology, The Affiliated Huai'an No.1 People's Hospital of Nanjing Medical University, Huai'an, China.
Rui XieDepartment of Gastroenterology, The Affiliated Huai'an No.1 People's Hospital of Nanjing Medical University, Huai'an, China.
ShaoChuang WangDepartment of Hepatobiliary & Pancreatic Surgery, The Affiliated Huai'an No.1 People's Hospital of Nanjing Medical University, Huai'an, China.ORCID 0000-0003-1043-1798
Wu JiDepartment of General Surgery, Jinling Clinical Medical College, Nanjing Medical University, Nanjing, China.ORCID 0000-0001-9328-1662
Xuzhou Medical College · CNNanjing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The interaction between Axin and DVL2 is critical for the breaking down of the beta-catenin destruction complex and the activation of the Wnt/beta-catenin cascade. However, this biological process remains poorly understood. In the present study, TM4SF1 was identified as the interacting partner of DVL2 and positively regulated as Wnt/beta-catenin signalling by strengthening the DVL2-Axin interaction. The expression levels of TM4SF1 were elevated in hepatocellular carcinoma (HCC) and were induced by Kras signalling. The overexpression of TM4SF1 promoted the growth and motility of HCC cells, and up-regulated the target genes (Axin2 and cyclin D1). The down-regulation of TM4SF1 impaired the capability of HCC cells for growth, migration and metastasis. In addition, the down-regulation of TM4SF1 promoted the ubiquitination of beta-catenin. In summary, these results reveal the oncogenic functions of TM4SF1 in HCC progression and suggest that TM4SF1 might be a target for treatment.

Indexed as

Signal TransductionAnimalsAntigens, Surfacebeta CateninBiomarkersCarcinoma, HepatocellularCell Line, TumorCell MovementCell ProliferationDisease Models, AnimalDisease SusceptibilityDishevelled ProteinsGene ExpressionHumansImmunohistochemistryLiver NeoplasmsAntigens, Surfacebeta CateninBiomarkersDishevelled ProteinsDVL2 protein, humanNeoplasm ProteinsTCF Transcription FactorsTM4SF1 protein, humanhepatocellular carcinomamigration and metastasisTM4SF1Wnt/beta-catenin cascade

Identifiers

PMID31876386
PMCPMC7933925
OpenAlexW2997945885

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Registered trials

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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.