Evidence map›Paper›PMID 29235470›Full record

ArticleCell death & disease2017

Upregulation of B7-H4 promotes tumor progression of intrahepatic cholangiocarcinoma.

Nan Xie, Jia-Bin Cai, Lu Zhang, Peng-Fei Zhang, Ying-Hao Shen, Xuan Yang, Jia-Cheng Lu, Dong-Mei Gao, Qiang Kang, Li-Xin Liu and 9 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell death & disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 1 pooled it
3.7field-weighted citation impact, top 7% 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

35 citing papers in PubMed, 1 synthesis or guideline pooled it, 64 citations in OpenAlex.

  1. Pooled it
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  6. 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

19 authors at 4 institutions in 1 country.

Nan XieKey Laboratory of Carcinogenesis and Cancer Invasion of Chinese Ministry, Department of Liver Surgery and Liver Transplant of Zhongshan Hospital, Liver Cancer Institute of Fudan University, Fudan University, Shanghai, 200032, China.
Jia-Bin CaiKey Laboratory of Carcinogenesis and Cancer Invasion of Chinese Ministry, Department of Liver Surgery and Liver Transplant of Zhongshan Hospital, Liver Cancer Institute of Fudan University, Fudan University, Shanghai, 200032, China.
Lu ZhangKey Laboratory of Carcinogenesis and Cancer Invasion of Chinese Ministry, Department of Liver Surgery and Liver Transplant of Zhongshan Hospital, Liver Cancer Institute of Fudan University, Fudan University, Shanghai, 200032, China.
Peng-Fei ZhangKey Laboratory of Carcinogenesis and Cancer Invasion of Chinese Ministry, Department of Liver Surgery and Liver Transplant of Zhongshan Hospital, Liver Cancer Institute of Fudan University, Fudan University, Shanghai, 200032, China.
Ying-Hao ShenKey Laboratory of Carcinogenesis and Cancer Invasion of Chinese Ministry, Department of Liver Surgery and Liver Transplant of Zhongshan Hospital, Liver Cancer Institute of Fudan University, Fudan University, Shanghai, 200032, China.
Xuan YangKey Laboratory of Carcinogenesis and Cancer Invasion of Chinese Ministry, Department of Liver Surgery and Liver Transplant of Zhongshan Hospital, Liver Cancer Institute of Fudan University, Fudan University, Shanghai, 200032, China.
Jia-Cheng LuKey Laboratory of Carcinogenesis and Cancer Invasion of Chinese Ministry, Department of Liver Surgery and Liver Transplant of Zhongshan Hospital, Liver Cancer Institute of Fudan University, Fudan University, Shanghai, 200032, China.
Dong-Mei GaoKey Laboratory of Carcinogenesis and Cancer Invasion of Chinese Ministry, Department of Liver Surgery and Liver Transplant of Zhongshan Hospital, Liver Cancer Institute of Fudan University, Fudan University, Shanghai, 200032, China.
Qiang KangDepartment of Hepatopancreatobiliary Surgery, The Second Affiliated Hospital of Kunming Medical University, Kunming, Yunnan, 650101, China.
Li-Xin LiuDepartment of Hepatopancreatobiliary Surgery, The Second Affiliated Hospital of Kunming Medical University, Kunming, Yunnan, 650101, China.
Chi ZhangKey Laboratory of Carcinogenesis and Cancer Invasion of Chinese Ministry, Department of Liver Surgery and Liver Transplant of Zhongshan Hospital, Liver Cancer Institute of Fudan University, Fudan University, Shanghai, 200032, China.
Xiao-Yong HuangKey Laboratory of Carcinogenesis and Cancer Invasion of Chinese Ministry, Department of Liver Surgery and Liver Transplant of Zhongshan Hospital, Liver Cancer Institute of Fudan University, Fudan University, Shanghai, 200032, China.
Hao ZouDepartment of Hepatopancreatobiliary Surgery, The Second Affiliated Hospital of Kunming Medical University, Kunming, Yunnan, 650101, China.
Xin-Yu ZhangKey Laboratory of Carcinogenesis and Cancer Invasion of Chinese Ministry, Department of Liver Surgery and Liver Transplant of Zhongshan Hospital, Liver Cancer Institute of Fudan University, Fudan University, Shanghai, 200032, China.
Zheng-Ji SongDepartment of Gastroenterology, The First People's Hospital of Yunnan Province, 157 Jin Bi Road, Kunming, Yunnan, 650032, China.
Hai-Xiang SunKey Laboratory of Carcinogenesis and Cancer Invasion of Chinese Ministry, Department of Liver Surgery and Liver Transplant of Zhongshan Hospital, Liver Cancer Institute of Fudan University, Fudan University, Shanghai, 200032, China.
Bi-Mang FuDepartment of Hepatopancreatobiliary Surgery, The Second Affiliated Hospital of Kunming Medical University, Kunming, Yunnan, 650101, China. fubimang@163.com.
Ai-Wu KeKey Laboratory of Carcinogenesis and Cancer Invasion of Chinese Ministry, Department of Liver Surgery and Liver Transplant of Zhongshan Hospital, Liver Cancer Institute of Fudan University, Fudan University, Shanghai, 200032, China. ke.aiwu@zs-hospital.sh.cn.
Guo-Ming ShiKey Laboratory of Carcinogenesis and Cancer Invasion of Chinese Ministry, Department of Liver Surgery and Liver Transplant of Zhongshan Hospital, Liver Cancer Institute of Fudan University, Fudan University, Shanghai, 200032, China. shi.guoming@zs-hospital.sh.cn.
Zhongshan Hospital · CNFudan University · CNKunming Medical University · CNFirst People's Hospital of Yunnan Province · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent reports show that B7-H4 is highly expressed in a variety of tumor cells, functions as a negative regulator of T cells and then promotes tumor progression. However, its expression and role in intrahepatic cholangiocarcinoma (ICC) remain unclear. In present study, B7-H4 expression in ICC and peritumoral tissues was determined at the level of mRNA and protein, and its bioactivity in ICC cells was studied after modification of B7-H4 expression. Then, the mechanism related to tumor progression induced by B7-H4 expression in ICC cells was explored. Finally, clinical significance of B7-H4 expression in ICC patients was further analyzed. The results showed that B7-H4 expression in ICC was much higher than that in peritumoral tissues at the level of both mRNA and protein. The high level of B7-H4 in ICC cells induced epithelial-to-mesenchymal transitions and promoted invasion and metastasis of tumor cells through activation of ERK1/2 signaling. The elevated B7-H4 expression was associated with the downregulated Bax, upregulated Bcl-2 expression, and activation of caspase-3. Clinically, high B7-H4 expression in tumor samples was significantly related to malignant phenotype, such as lymph node metastasis, high tumor stage, and poor differentiation. ICC patients with high expression of B7-H4 had shorter overall survival (OS) and disease-free survival. Moreover, the B7-H4 expression was an independent prognostic factor for predicting OS and tumor recurrence of ICC patients after operation. In conclusion, high expression of B7-H4 promotes tumor progression of ICC and may be a novel therapeutic target for ICC patients.

Indexed as

Gene Expression Regulation, NeoplasticAdultAgedbcl-2-Associated X ProteinBile Duct NeoplasmsBiomarkers, TumorCaspase 3CholangiocarcinomaDisease ProgressionEpithelial-Mesenchymal TransitionFemaleHumansLymphatic MetastasisMaleMiddle AgedMitogen-Activated Protein Kinase 1BAX protein, humanbcl-2-Associated X ProteinBCL2 protein, humanBiomarkers, TumorCASP3 protein, humanCaspase 3MAPK1 protein, humanMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Proto-Oncogene Proteins c-bcl-2V-Set Domain-Containing T-Cell Activation Inhibitor 1VTCN1 protein, human

Identifiers

PMID29235470
PMCPMC5870586
OpenAlexW2773597902

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.