Evidence map›Paper›PMID 35384345›Full record

ArticleClinical and translational medicine2022

CD155/SRC complex promotes hepatocellular carcinoma progression via inhibiting the p38 MAPK signalling pathway and correlates with poor prognosis.

An-Li Jin, Chun-Yan Zhang, Wen-Jing Zheng, Jing-Rong Xian, Wen-Jing Yang, Te Liu, Wei Chen, Tong Li, Bei-Li Wang, Bai-Shen Pan and 8 more

Open access · goldAbstract read
In one paragraph

Article in Clinical and translational medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 1 pooled it
3.4field-weighted citation impact, top 6% 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

25 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Emerging Immune-Based Therapeutic Strategies in Hepatocellular Carcinoma.Liver international : official journal of the International Association for the Study of the Liver · 2026
    Review
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  16. CTLA-4 silencing could promote anti-tumor effects in hepatocellular.Medical oncology (Northwood, London, England) · 2024
    Article
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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 3 institutions in 2 countries.

An-Li JinDepartment of Laboratory Medicine, Zhongshan Hospital, Fudan University, Shanghai, P. R. China.
Chun-Yan ZhangDepartment of Laboratory Medicine, Zhongshan Hospital, Fudan University, Shanghai, P. R. China.
Wen-Jing ZhengDepartment of Liver Surgery & Transplantation, Liver Cancer Institute, Zhongshan Hospital, Fudan University, Key Laboratory of Carcinogenesis and Cancer Invasion, Ministry of Education, Shanghai, P. R. China.
Jing-Rong XianDepartment of Laboratory Medicine, Zhongshan Hospital, Fudan University, Shanghai, P. R. China.
Wen-Jing YangDepartment of Laboratory Medicine, Zhongshan Hospital, Fudan University, Shanghai, P. R. China.
Te LiuDepartment of Laboratory Medicine, Zhongshan Hospital, Fudan University, Shanghai, P. R. China.
Wei ChenDepartment of Laboratory Medicine, Zhongshan Hospital, Fudan University, Shanghai, P. R. China.
Tong LiDepartment of Laboratory Medicine, Zhongshan Hospital, Fudan University, Shanghai, P. R. China.
Bei-Li WangDepartment of Laboratory Medicine, Zhongshan Hospital, Fudan University, Shanghai, P. R. China.ORCID 0000-0001-5167-170X
Bai-Shen PanDepartment of Laboratory Medicine, Zhongshan Hospital, Fudan University, Shanghai, P. R. China.
Qian LiDepartment of Laboratory Medicine, Zhongshan Hospital, Fudan University, Shanghai, P. R. China.
Jian-Wen ChengDepartment of Liver Surgery & Transplantation, Liver Cancer Institute, Zhongshan Hospital, Fudan University, Key Laboratory of Carcinogenesis and Cancer Invasion, Ministry of Education, Shanghai, P. R. China.
Peng-Xiang WangDepartment of Liver Surgery & Transplantation, Liver Cancer Institute, Zhongshan Hospital, Fudan University, Key Laboratory of Carcinogenesis and Cancer Invasion, Ministry of Education, Shanghai, P. R. China.
Bo HuDepartment of Liver Surgery & Transplantation, Liver Cancer Institute, Zhongshan Hospital, Fudan University, Key Laboratory of Carcinogenesis and Cancer Invasion, Ministry of Education, Shanghai, P. R. China.
Jian ZhouDepartment of Liver Surgery & Transplantation, Liver Cancer Institute, Zhongshan Hospital, Fudan University, Key Laboratory of Carcinogenesis and Cancer Invasion, Ministry of Education, Shanghai, P. R. China.
Jia FanDepartment of Liver Surgery & Transplantation, Liver Cancer Institute, Zhongshan Hospital, Fudan University, Key Laboratory of Carcinogenesis and Cancer Invasion, Ministry of Education, Shanghai, P. R. China.
Xin-Rong YangDepartment of Liver Surgery & Transplantation, Liver Cancer Institute, Zhongshan Hospital, Fudan University, Key Laboratory of Carcinogenesis and Cancer Invasion, Ministry of Education, Shanghai, P. R. China.ORCID 0000-0002-2716-9338
Wei GuoDepartment of Laboratory Medicine, Zhongshan Hospital, Fudan University, Shanghai, P. R. China.ORCID 0000-0003-4406-1094
Sun Yat-sen University · CNFudan University · CNShenzhen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundHepatocellular carcinoma (HCC) is a prevalent malignancy with poor prognosis. As a cell adhesion molecule, poliovirus receptor (PVR/CD155) is abnormally overexpressed in tumour cells, and related to tumour proliferation and invasion. However, the potential role and mechanism of CD155 have not yet been elucidated in HCC.

methodsImmunohistochemistry, RT-PCR and Western blot assays were used to determine CD155 expression in HCC cell lines and tissues. Cell Counting Kit-8 and colony formation assays were used to examine cell proliferation. Transwell and wound healing assays were used to evaluate cell migration and invasion. Cell apoptosis and cycle distribution were assessed by flow cytometry. Cox regression and Kaplan-Meier analyses were performed to explore the clinical significance of CD155. The role of CD155 in vivo was evaluated by establishing liver orthotropic xenograft mice model. RNA sequencing, bioinformatics analysis and co-immunoprecipitation assay were used to explore the downstream signalling pathway of CD155.

resultsCD155 was upregulated in HCC tissues and represented a promising prognostic indicator for HCC patients (n = 189) undergoing curative resection. High CD155 expression enhanced cell proliferation, migration and invasion, and contributed to cell survival in HCC. CD155 overexpression also induced epithelial-mesenchymal transition in HCC cells. CD155 function in HCC involved SRC/p38 MAPK signalling pathway. CD155 interacted with SRC homology-2 domain of SRC and promoted SRC activation, further inhibiting the downstream p38 MAPK signalling pathway in HCC.

conclusionsCD155 promotes HCC progression via the SRC/p38 MAPK signalling pathway. CD155 may represent a predictor for poor postsurgery prognosis in HCC patients.

Indexed as

Carcinoma, HepatocellularLiver NeoplasmsMAP Kinase Signaling SystemReceptors, VirusAnimalsHumansMicep38 Mitogen-Activated Protein KinasesPrognosisp38 Mitogen-Activated Protein Kinasespoliovirus receptorReceptors, Virusepithelial-mesenchymal transitionhepatocellular carcinomapoliovirus receptorprognosisSRC

Identifiers

PMID35384345
PMCPMC8982318
OpenAlexW4223449336

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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.