Evidence map›Paper›PMID 25908926›Full record

ArticleCancer cell international2015

B7-H3 promotes aggression and invasion of hepatocellular carcinoma by targeting epithelial-to-mesenchymal transition via JAK2/STAT3/Slug signaling pathway.

Fu-Biao Kang, Ling Wang, Heng-Chuan Jia, Dong Li, Hai-Jun Li, Yin-Ge Zhang, Dian-Xing Sun

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Cancer cell international, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 108 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
108citing papers in PubMed, 1 pooled it
6.0field-weighted citation impact, top 3% 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

108 citing papers in PubMed, 1 synthesis or guideline pooled it, 156 citations in OpenAlex.

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  19. B7-H3 suppresses CD8Journal of Cancer · 2024
    Article
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48 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 3 institutions in 1 country.

Fu-Biao Kang *Department of Liver Diseases, Bethune International Peace Hospital, Shijiazhuang, Hebei People's Republic of China.
Ling Wang *Cancer Research Institute, the Fourth Hospital of Hebei Medical University, Shijiazhuang, Hebei People's Republic of China.
Heng-Chuan Jia *Department of Liver Diseases, Bethune International Peace Hospital, Shijiazhuang, Hebei People's Republic of China.
Dong LiDepartment of Liver Diseases, Bethune International Peace Hospital, Shijiazhuang, Hebei People's Republic of China.
Hai-Jun LiDepartment of Liver Diseases, Bethune International Peace Hospital, Shijiazhuang, Hebei People's Republic of China.
Yin-Ge ZhangDepartment of Liver Diseases, Bethune International Peace Hospital, Shijiazhuang, Hebei People's Republic of China.
Dian-Xing SunDepartment of Liver Diseases, Bethune International Peace Hospital, Shijiazhuang, Hebei People's Republic of China.
Bethune International Peace Hospital · CNChinese PLA General Hospital · CNFourth Hospital of Hebei Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundB7-homologue 3 (B7-H3), a recently identified immunoregulatory protein, has been shown to be overexpressed in human hepatocellular carcinoma (HCC). However, whether the dynamic expression pattern of B7-H3 contributes to early invasion of HCC is largely unknown. In addition, the biological roles of B7-H3 in HCC are still unclear. Herein, we are going to examine B7-H3 expression profile and its clinicopathological significance in primary and metastatic HCC, and further determine whether B7-H3 knockdown simulates different pathological states of HCC progression and metastasis.

methodsUsing immunohistochemistry, B7-H3 expression was studied on 116 HCC containing primary and metastatic HCCs. Survival curves and log-rank tests were used to test the association of B7-H3 expression with survival. HCC cells with B7-H3 depletion were established by RNA interference to investigate the effect of B7-H3 on cell proliferation, apoptosis, migration and invasion in vitro.

resultsStatistical analysis of clinical cases revealed that B7-H3 high expression group had inclinations towards late TNM stage, the presence of vascular invasion, lymph metastasis, and the formation of microsatellite tumors. Increased intensity of tumor B7-H3 staining was detected more significantly in metastatic HCC tumors. Consistently in experiments performed in vitro, B7-H3 was able to stimulate the wound healing, metastasis and invasion of hepatoma cells by targeting epithelial-to-mesenchymal transition (EMT) via JAK2/Stat3/Slug signaling pathway, while no obvious influence on cell growth and apoptosis.

conclusionB7-H3 in the regulation of the metastatic capacity of HCC cells makes itself a promising therapeutic target for anti-metastasis therapy.

Indexed as

B7-H3Epithelial-To-Mesenchymal TransitionHepatocellular carcinomaInvasionJAK/STAT signaling pathway

Identifiers

PMID25908926
PMCPMC4407415
OpenAlexW2097419166

What OpenQuestion holds

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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.