Evidence map›Paper›PMID 40750784›Full record

ArticleCell death & disease2025

SORT1 promote the metastasis and invasion of hepatocellular carcinoma via p38/β-catenin/ZEB1 signaling pathway.

Hongjie Chen, Wei Liao, Yuanhui Jiang, Guichan Liao, Xinrui Gao, Siyi Cen, Lili Liu, Jie Peng, Cai Shaohang

Abstract read
In one paragraph

Article in Cell death & disease, 2025. 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

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

2 citing papers in PubMed.

  1. Review
  2. Review
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.

Hongjie Chen *State Key Laboratory of Organ Failure Research, Guangdong Provincial Key Laboratory of Viral Hepatitis Research, Key Laboratory of Infectious Diseases Research in South China, Department of Infectious Diseases, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Wei Liao *Department of Intensive Care Unit, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center, Guangzhou, China.
Yuanhui Jiang *State Key Laboratory of Organ Failure Research, Guangdong Provincial Key Laboratory of Viral Hepatitis Research, Key Laboratory of Infectious Diseases Research in South China, Department of Infectious Diseases, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Guichan LiaoState Key Laboratory of Organ Failure Research, Guangdong Provincial Key Laboratory of Viral Hepatitis Research, Key Laboratory of Infectious Diseases Research in South China, Department of Infectious Diseases, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Xinrui GaoState Key Laboratory of Organ Failure Research, Guangdong Provincial Key Laboratory of Viral Hepatitis Research, Key Laboratory of Infectious Diseases Research in South China, Department of Infectious Diseases, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Siyi CenSouthern Medical University, Guangzhou, China.
Lili LiuDepartment of Pathology, State Key Laboratory of Oncology in South China, Sun Yat-sen University Cancer Center, Guangzhou, China. liulil@sysucc.org.cn.ORCID http://orcid.org/0000-0002-4347-2038
Jie PengState Key Laboratory of Organ Failure Research, Guangdong Provincial Key Laboratory of Viral Hepatitis Research, Key Laboratory of Infectious Diseases Research in South China, Department of Infectious Diseases, Nanfang Hospital, Southern Medical University, Guangzhou, China. pjie138@163.com.ORCID http://orcid.org/0000-0003-0928-3134
Cai ShaohangState Key Laboratory of Organ Failure Research, Guangdong Provincial Key Laboratory of Viral Hepatitis Research, Key Laboratory of Infectious Diseases Research in South China, Department of Infectious Diseases, Nanfang Hospital, Southern Medical University, Guangzhou, China. shaohangcai@foxmail.com.ORCID http://orcid.org/0000-0003-3765-9127

Funding

National Natural Science Foundation of China (National Science Foundation of China) 82203300
6 · The paper itself

Abstract

Metastasis is the predominant reason for high mortality of hepatocellular carcinoma (HCC) patients. Understanding the molecular mechanisms underlying HCC metastases is critical. Here, we reported that SORT1 functioned as an oncogene by facilitating HCC metastasis. Elevated SORT1 expression was positively correlated with increased tumor number, advanced TNM stage, and vascular invasion. Mechanistically, SORT1 binds to p38 and enhances its stability. Furthermore, p38 phosphorylates GSK-3β at Ser9, which promotes nuclear accumulation of β-catenin, leading to the transcription of ZEB1 and secretion of exosomes. Knockdown of SORT1 and ZEB1 inhibited HCC metastasis, whereas upregulation of ZEB1 restored SORT1 knockdown-induced suppression of HCC metastasis. SORT1 expression was positively correlated with Sterol regulatory element-binding proteins 2 (SREBP2) and ZEB1 expression in human HCC tissues. In light of these results, SORT1 as a potential prognostic biomarker in HCC and targeting WNT/β-catenin signaling pathway, could be an effective therapeutic strategy against HCC metastasis.

Indexed as

beta CateninCarcinoma, HepatocellularLiver Neoplasmsp38 Mitogen-Activated Protein KinasesZinc Finger E-box-Binding Homeobox 1AnimalsCell Line, TumorCell MovementFemaleGene Expression Regulation, NeoplasticGlycogen Synthase Kinase 3 betaHumansMaleMiceMice, Inbred BALB CMice, Nudebeta CateninGlycogen Synthase Kinase 3 betap38 Mitogen-Activated Protein KinasesZEB1 protein, humanZinc Finger E-box-Binding Homeobox 1

Identifiers

PMID40750784
PMCPMC12317026

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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.