Evidence mapPaperPMID 37547758Full record

ArticleOncology research2023

Zyxin promotes hepatocellular carcinoma progression via the activation of AKT/mTOR signaling pathway.

Tianying Cai, Junjie Bai, Peng Tan, Zhiwei Huang, Chen Liu, Ziming Wu, Yonglang Cheng, Tongxi Li, Yifan Chen, Jian Ruan and 3 more

Abstract read
In one paragraph

Article in Oncology research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing 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

7 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Down Expression of Zyxin is Associated with Down Expression of p53 in Colorectal Cancer.International journal of molecular and cellular medicine · 2025
    Article
  6. Article
  7. 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

13 authors.

Tianying CaiDepartment of Hepatobiliary Surgery, Affiliated Hospital of Southwest Medical University, Luzhou, 646000, China.
Junjie BaiDepartment of Hepatobiliary Surgery, Affiliated Hospital of Southwest Medical University, Luzhou, 646000, China.
Peng TanAcademician (Expert) Workstation of Sichuan Province, The Affiliated Hospital of Southwest Medical University, Luzhou, 646000, China.
Zhiwei HuangDepartment of Hepatobiliary Surgery, Affiliated Hospital of Southwest Medical University, Luzhou, 646000, China.
Chen LiuDepartment of Hepatobiliary Surgery, Affiliated Hospital of Southwest Medical University, Luzhou, 646000, China.
Ziming WuDepartment of Hepatobiliary Surgery, Affiliated Hospital of Southwest Medical University, Luzhou, 646000, China.
Yonglang ChengDepartment of Hepatobiliary Surgery, Affiliated Hospital of Southwest Medical University, Luzhou, 646000, China.
Tongxi LiDepartment of Hepatobiliary Surgery, Affiliated Hospital of Southwest Medical University, Luzhou, 646000, China.
Yifan ChenDepartment of Hepatobiliary Surgery, Affiliated Hospital of Southwest Medical University, Luzhou, 646000, China.
Jian RuanDepartment of Medical Oncology, First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, 310000, China.
Lin GaoDepartment of Health Management, The Affiliated Hospital of Southwest Medical University, Luzhou, 646000, China.
Yichao DUAcademician (Expert) Workstation of Sichuan Province, The Affiliated Hospital of Southwest Medical University, Luzhou, 646000, China.
Wenguang FuDepartment of Hepatobiliary Surgery, Affiliated Hospital of Southwest Medical University, Luzhou, 646000, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatocellular carcinoma (HCC) is a common malignancy that is driven by multiple genes and pathways. The aim of this study was to investigate the role and specific mechanism of the actin-interacting protein zyxin (ZYX) in HCC. We found that the expression of ZYX was significantly higher in HCC tissues compared to that in normal liver tissues. In addition, overexpression of ZYX in hepatoma cell lines (PLC/PRF/5, HCCLM3) enhanced their proliferation, migration and invasion, whereas ZYX knockdown had the opposite effects (SK HEP-1, Huh-7). Furthermore, the change in the expression levels of ZYX also altered that of proteins related to cell cycle, migration and invasion. Similar results were obtained with xenograft models. The AKT/mTOR signaling pathway is one of the key mediators of cancer development. While ZYX overexpression upregulated the levels of phosphorylated AKT/mTOR proteins, its knockdown had the opposite effect. In addition, the AKT inhibitor MK2206 neutralized the pro-oncogenic effects of ZYX on the HCC cells, whereas the AKT activator SC79 restored the proliferation, migration and invasion of HCC cells with ZYX knockdown. Taken together, ZYX promotes the malignant progression of HCC by activating AKT/mTOR signaling pathway, and is a potential therapeutic target in HCC.

Indexed as

Carcinoma, HepatocellularLiver NeoplasmsZyxinCell Line, TumorCell MovementCell ProliferationHumansProto-Oncogene Proteins c-aktSignal TransductionTOR Serine-Threonine KinasesProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesZyxinZYX protein, humanAKT/mTORHepatocellular carcinomaInvasionMigrationProliferationZyxin

Identifiers

PMID37547758
PMCPMC10398406

What Socratic holds

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LicenceCC BY
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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 Socratic graph.