Evidence map›Paper›PMID 39073023›Full record

ArticleCancer communications (London, England)2024

Galectin 3-binding protein (LGALS3BP) depletion attenuates hepatic fibrosis by reducing transforming growth factor-β1 (TGF-β1) availability and inhibits hepatocarcinogenesis.

Dae-Hwan Kim, Minjeong Sung, Myong-Suk Park, Eun-Gene Sun, Sumin Yoon, Kyung Hyun Yoo, Kamalakannan Radhakrishnan, Sung Yun Jung, Woo-Kyun Bae, Sang-Hee Cho and 1 more

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In one paragraph

Article in Cancer communications (London, England), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing 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

21 citing papers in PubMed.

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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

11 authors.

Dae-Hwan KimDepartment of Internal Medicine, Division of Hematology and Oncology, Chonnam National University Medical School, Hwasun, South Korea.
Minjeong SungDepartment of Internal Medicine, Division of Hematology and Oncology, Chonnam National University Medical School, Hwasun, South Korea.
Myong-Suk ParkDepartment of Internal Medicine, Division of Hematology and Oncology, Chonnam National University Medical School, Hwasun, South Korea.
Eun-Gene SunDepartment of Internal Medicine, Division of Hematology and Oncology, Chonnam National University Medical School, Hwasun, South Korea.
Sumin YoonDepartment of Biological Science, Sookmyung Women's University, Seoul, South Korea.
Kyung Hyun YooDepartment of Biological Science, Sookmyung Women's University, Seoul, South Korea.ORCID 0000-0003-2172-5564
Kamalakannan RadhakrishnanClinical Vaccine R&D Center, Chonnam National University, Hwasun, South Korea.
Sung Yun JungDepartment of Biochemistry and Molecular Pharmacology, Baylor College of Medicine, Houston, Texas, USA.
Woo-Kyun BaeDepartment of Internal Medicine, Division of Hematology and Oncology, Chonnam National University Medical School, Hwasun, South Korea.
Sang-Hee ChoDepartment of Internal Medicine, Division of Hematology and Oncology, Chonnam National University Medical School, Hwasun, South Korea.
Ik-Joo ChungDepartment of Internal Medicine, Division of Hematology and Oncology, Chonnam National University Medical School, Hwasun, South Korea.ORCID 0000-0003-0479-8067

Funding

Bio & Medical Technology Development Program of the National Research Foundation NRF-2020M3A9G3080281Bio & Medical Technology Development Program of the National Research Foundation NRF-2020R1A5A2031185Korean Government
6 · The paper itself

Abstract

backgroundIncreased Galectin 3-binding protein (LGALS3BP) serum levels have been used to assess hepatic fibrosis stages and the severity of hepatocellular carcinoma (HCC). Considering the crucial role of transforming growth factor-β1 (TGF-β1) in the emergence of these diseases, the present study tested the hypothesis that LGALS3BP regulates the TGF-β1 signaling pathway.

methodsThe expression levels of LGALS3BP and TGFB1 were analyzed in patients with metabolic dysfunction-associated steatohepatitis (MASH) and HCC. Multiple omics techniques, such as RNA-sequencing, transposase-accessible chromatin-sequencing assay, and liquid chromatography-tandem mass spectrometry proteomics, were used to identify the regulatory mechanisms for the LGALS3BP-TGF-β1 axis. The effects of altered TGF-β1 signaling by LGALS3BP were investigated in conditional LGALS3BP-knockin and LGALS3BP-knockout mice.

resultsIn patients with MASH and HCC, the levels of LGALS3BP and TGFB1 exhibited positive correlations. Stimulation of LGALS3BP by the inflammatory cytokine interferon α in HCC cells or ectopic overexpression of LGALS3BP in hepatocytes promoted the expression levels of TGFB1. Aggravated fibrosis was observed in the livers of hepatocyte-specific LGALS3BP-knockin mice, with increased TGFB1 levels. LGALS3BP directly bound to and assembled integrin αV, an integral mediator required for releasing active TGF-β1 from extracellular latent complex with the rearranged F-actin cytoskeleton. The released TGF-β1 activated JunB transcription factor, which in turn promoted the TGF-β1 positive feedback loop. LGALS3BP deletion in the hepatocytes downregulated TGF-β1 signaling and CCl

conclusionLGALS3BP plays a crucial role in hepatic fibrosis and carcinogenesis by controlling the TGF-β1 signaling pathway, making it a promising therapeutic target in TGF-β1-related diseases.

Indexed as

Carcinoma, HepatocellularLiver CirrhosisLiver NeoplasmsAnimalsAntigens, NeoplasmCarcinogenesisCarrier ProteinsExtracellular Matrix ProteinsFemaleHumansMaleMiceMice, Inbred C57BLMice, KnockoutSignal TransductionTransforming Growth Factor beta1Antigens, NeoplasmCarrier ProteinsExtracellular Matrix ProteinsLGALS3BP protein, humanTGFB1 protein, humanTransforming Growth Factor beta1F‐actinFAKhepatic carcinogenesisIntegrin αVInterferon αJunBLGALS3BPmetabolic dysfuntion‐associated steatohepatitistensile forceTGF‐β1

Identifiers

PMID39073023
PMCPMC11483554

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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.