Evidence map›Paper›PMID 39714087›Full record

ArticlePhysiological reports2024

Zbtb7b defines a compensatory mechanism in MASLD-related HCC progression by suppressing H19-mediated hepatic lipid deposition.

Yinglin Han, Kaimin Wu, Xin Peng, Yinkun Fu, Wenyan Li, Jing Ma, He Jiang, Xu-Yun Zhao

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Physiological reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

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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

2 citing papers in PubMed.

  1. Review
  2. 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

8 authors.

Yinglin HanDepartment of Biochemistry and Molecular Cell Biology, Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Key Laboratory of Cell Differentiation and Apoptosis of National Ministry of Education, Shanghai Jiao Tong University School of Medicine, Shanghai, China.ORCID 0009-0004-4860-1355
Kaimin WuDepartment of Biochemistry and Molecular Cell Biology, Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Key Laboratory of Cell Differentiation and Apoptosis of National Ministry of Education, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Xin PengDepartment of Biochemistry and Molecular Cell Biology, Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Key Laboratory of Cell Differentiation and Apoptosis of National Ministry of Education, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Yinkun FuDepartment of Pathophysiology, Key Laboratory of Cell Differentiation and Apoptosis of Ministry of Education, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Wenyan LiDepartment of Biochemistry and Molecular Cell Biology, Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Key Laboratory of Cell Differentiation and Apoptosis of National Ministry of Education, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Jing MaDepartment of Endocrinology and Metabolism, Renji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
He JiangLiver Cancer Institute, Zhongshan Hospital, Fudan University, Shanghai Medical College, Shanghai, China.
Xu-Yun ZhaoDepartment of Biochemistry and Molecular Cell Biology, Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Key Laboratory of Cell Differentiation and Apoptosis of National Ministry of Education, Shanghai Jiao Tong University School of Medicine, Shanghai, China.ORCID 0000-0002-0949-3409

Funding

Innovative research team of high-level local universities of Shanghai SHSMU-ZDCX20212501MOST | National Key Research and Development Program of China (NKPs) 2020YFA0803603MOST | National Key Research and Development Program of China (NKPs) 2023YFA1800802National Natural Science Foundation of China (NSFC) 82070894Science and Technology Commission of Shanghai Municipality (STCSM) 22ZR1479800
6 · The paper itself

Abstract

Hepatocellular carcinoma (HCC) is a widely prevalent type of primary liver cancer. However, strategies for pretumor intervention are still limited. In this study, a liver-specific Zbtb7b knockout mouse model was used to evaluate the role of Zbtb7b in metabolic dysfunction-associated steatotic liver disease (MASLD)-related HCC development. We revealed that Zbtb7b was compensatively increased and restricted lipid deposition in the liver during MASLD progression, which protects against MASLD-related HCC initiation. Mechanistically, Zbtb7b suppresses the expression of the long noncoding RNA H19 to attenuate hepatic de novo lipogenesis and increase fatty acid oxidation, thereby preventing lipid accumulation in hepatocytes. As a result, the proliferation and migration abilities of HCC cells are reduced. Overall, we demonstrated that Zbtb7b serves as a tumor suppressor at an early stage of HCC, thus providing a promising target for the treatment of HCC at a premalignant stage.

Indexed as

Carcinoma, HepatocellularLiver NeoplasmsRNA, Long NoncodingAnimalsCell Line, TumorCell ProliferationDisease ProgressionDNA-Binding ProteinsFatty LiverHumansLipid MetabolismLiverMaleMiceMice, Inbred C57BLMice, KnockoutDNA-Binding ProteinsH19 long non-coding RNARNA, Long NoncodingTranscription Factorsde novo lipogenesisfatty acid oxidationH19hepatocellular carcinomametabolic dysfunction‐associated steatotic liver diseaseZbtb7b

Identifiers

PMID39714087
PMCPMC11664540

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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.