Evidence map›Paper›PMID 30719823›Full record

ArticleCancer science2019

Krüppel-like factor 2 inhibits hepatocarcinogenesis through negative regulation of the Hedgehog pathway.

JinBo Lin, Huifang Tan, Yingjie Nie, Dongwen Wu, Weiji Zheng, Wensong Lin, Zheng Zhu, Bing Yang, Xiaoliang Chen, Tao Chen

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cancer science, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

22 citing papers in PubMed, 48 citations in OpenAlex.

  1. Review
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  4. Deciphering the role ofWorld journal of hepatology · 2025
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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

10 authors at 5 institutions in 1 country.

JinBo LinLonggang Central Hospital of Shenzhen, Affiliated Longgang Hospital of Zunyi Medical University, Shenzhen, China.
Huifang TanThe First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.
Yingjie NieClinical Research Lab Center, Guizhou Provincial People's Hospital, Guiyang, China.
Dongwen WuThe Third Xiangya Hospital, Central South University, Changsha, China.
Weiji ZhengLonggang Central Hospital of Shenzhen, Affiliated Longgang Hospital of Zunyi Medical University, Shenzhen, China.
Wensong LinLonggang Central Hospital of Shenzhen, Affiliated Longgang Hospital of Zunyi Medical University, Shenzhen, China.
Zheng ZhuLonggang Central Hospital of Shenzhen, Affiliated Longgang Hospital of Zunyi Medical University, Shenzhen, China.
Bing YangLonggang Central Hospital of Shenzhen, Affiliated Longgang Hospital of Zunyi Medical University, Shenzhen, China.
Xiaoliang ChenShenzhen Guangming District Center for Disease Control and Prevention, Guangdong, China.
Tao ChenThe First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.ORCID https://orcid.org/0000-0002-8433-2509
Zunyi Medical University · CNFirst Affiliated Hospital of Guangzhou Medical University · CNCentral South University · CNGuizhou Provincial People's Hospital · CNShenzhen Center for Disease Control and Prevention · CN

Funding

Guangdong Provincial Department of Science and Technology 2018A030313525Guizhou Science and Technology Cooperation Platform 2017-5634Guizhou Science and Technology Cooperation Platform 2018-5801Science & Technology Department of Shenzhen Longgang District 20170403100420500
6 · The paper itself

Abstract

Hepatocellular carcinoma (HCC) is one of the most common malignancies worldwide. The most important reason for the occurrence of HCC is hepatitis C or B infection. Moreover, genetic factors play an important role in the tumorigenesis of HCC. Here, we demonstrated that Krüppel-like factor 2 (KLF2) expression was downregulated in HCC samples compared with adjacent tissues. Additionally, KLF2 was shown to inhibit the growth, migration and colony-formation ability of liver cancer cells. Further mechanistic studies revealed that KLF2 can compete with Gli1 for interaction with HDAC1 and restrains Hedgehog signal activation. Together, our results suggest that KLF2 has potential as a diagnostic biomarker and therapeutic target for the treatment of HCC.

Indexed as

Signal TransductionAnimalsCarcinoma, HepatocellularCell Line, TumorCell MovementCell ProliferationCell Transformation, NeoplasticDisease Models, AnimalGene Expression RegulationGenes, ReporterHedgehog ProteinsHumansKruppel-Like Transcription FactorsLiver NeoplasmsMaleMiceGLI1 protein, humanHedgehog ProteinsKLF2 protein, humanKruppel-Like Transcription FactorsZinc Finger Protein GLI1HDAC1Hedgehog signalinghepatocellular carcinomaintrahepatic metastasisKrüppel-like factor 2

Identifiers

PMID30719823
PMCPMC6447955
OpenAlexW2914391708

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.