Evidence map›Paper›PMID 34977001›Full record

ArticleFrontiers in cell and developmental biology2021

ITGB1 Drives Hepatocellular Carcinoma Progression by Modulating Cell Cycle Process Through PXN/YWHAZ/AKT Pathways.

Jinghe Xie, Tingting Guo, Zhiyong Zhong, Ning Wang, Yan Liang, Weiping Zeng, Shoupei Liu, Qicong Chen, Xianglian Tang, Haibin Wu and 8 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in cell and developmental biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.8field-weighted citation impact, top 8% 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

31 citing papers in PubMed, 44 citations in OpenAlex.

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  9. PPM1F regulates ovarian cancer progression by affecting the dephosphorylation of ITGB1.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025
    Article
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  13. Molecular docking andToxicology reports · 2024
    Article
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  17. Review
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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

18 authors at 4 institutions in 1 country.

Jinghe XieSchool of Biomedical Sciences and Engineering, Guangzhou International Campus, South China University of Technology, Guangzhou, China.
Tingting GuoLaboratory of Stem Cells and Translational Medicine, Institutes for Life Sciences and School of Medicine, South China University of Technology, Guangzhou, China.
Zhiyong ZhongSchool of Biomedical Sciences and Engineering, Guangzhou International Campus, South China University of Technology, Guangzhou, China.
Ning WangSchool of Biomedical Sciences and Engineering, Guangzhou International Campus, South China University of Technology, Guangzhou, China.
Yan LiangLaboratory of Stem Cells and Translational Medicine, Institutes for Life Sciences and School of Medicine, South China University of Technology, Guangzhou, China.
Weiping ZengSchool of Biology and Biological Engineering, South China University of Technology, Guangzhou, China.
Shoupei LiuLaboratory of Stem Cells and Translational Medicine, Institutes for Life Sciences and School of Medicine, South China University of Technology, Guangzhou, China.
Qicong ChenLaboratory of Stem Cells and Translational Medicine, Institutes for Life Sciences and School of Medicine, South China University of Technology, Guangzhou, China.
Xianglian TangSchool of Biomedical Sciences and Engineering, Guangzhou International Campus, South China University of Technology, Guangzhou, China.
Haibin WuLaboratory of Stem Cells and Translational Medicine, Institutes for Life Sciences and School of Medicine, South China University of Technology, Guangzhou, China.
Shuai ZhangDepartment of Gastroenterology and Hepatology, Guangzhou Digestive Disease Center, Guangzhou First People's Hospital, School of Medicine, South China University of Technology, Guangzhou, China.
Keqiang MaDepartment of Hepatobiliary Pancreatic Surgery, Huadu District People's Hospital of Guangzhou, Guangzhou, China.
Bailin WangDepartment of General Surgery, Guangzhou Red Cross Hospital, Jinan University, Guangzhou, China.
Yimeng OuDepartment of General Surgery, the First Affiliated Hospital of Guangdong Pharmaceutical University, Guangzhou, China.
Weili GuDepartment of Gastroenterology and Hepatology, Guangzhou Digestive Disease Center, Guangzhou First People's Hospital, School of Medicine, South China University of Technology, Guangzhou, China.
Honglin ChenLaboratory of Stem Cells and Translational Medicine, Institutes for Life Sciences and School of Medicine, South China University of Technology, Guangzhou, China.
Yaqi QiuLaboratory of Stem Cells and Translational Medicine, Institutes for Life Sciences and School of Medicine, South China University of Technology, Guangzhou, China.
Yuyou DuanLaboratory of Stem Cells and Translational Medicine, Institutes for Life Sciences and School of Medicine, South China University of Technology, Guangzhou, China.
South China University of Technology · CNGuangzhou Medical University · CNFirst Affiliated Hospital of Guangdong Pharmaceutical University · CNJinan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Integrin β1 (ITGB1), which acts as an extracellular matrix (ECM) receptor, has gained increasing attention as a therapeutic target for the treatment of hepatocellular carcinoma (HCC). However, the underpinning mechanism of how ITGB1 drives HCC progression remains elusive. In this study, we first found that ITGB1 expression was significantly higher in HCC tissues than in normal controls by bioinformatics analysis. Furthermore, bioinformatics analysis revealed that paxillin (PXN) and 14-3-3 protein zeta (YWHAZ) are the molecules participating in ITGB1-regulated HCC tumor cell cycle progression. Indeed, immunohistochemistry (IHC) revealed that ITGB1, paxillin, and YWHAZ were strongly upregulated in paired HCC tissue compared with adjacent normal tissues. Notably, the inhibition of ITGB1 expression by small interfering RNA (siRNA) resulted in the downregulated expression of PXN and YWHAZ in primary HCC cells, as assessed by western blot and immunostaining. In addition, ITGB1 knockdown markedly impaired the aggressive behavior of HCC tumor cells and delayed cell cycle progression as determined by cell migration assay, drug-resistance analysis, colony formation assay, quantitative real-time polymerase chain reaction (qRT-PCR), and cell cycle analysis as well as cell viability measurements. More importantly, we proved that xenograft ITGB1

Indexed as

14-3-3 protein zeta (YWHAZ)AKTcell cycle progressionhepatocellular carcinomaintegrin β1 (ITGB1)paxillin (PXN)

Identifiers

PMID34977001
PMCPMC8718767
OpenAlexW4200095628

What OpenQuestion 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 OpenQuestion graph.