Evidence map›Paper›PMID 30085405›Full record

ArticleCancer medicine2018

NFATc1 is a tumor suppressor in hepatocellular carcinoma and induces tumor cell apoptosis by activating the FasL-mediated extrinsic signaling pathway.

Sanrong Xu, Penghao Shu, Song Zou, Xiaofeng Shen, Yuanqian Qu, Yong Zhang, Kang Sun, Jin Zhang

Open access · goldAbstract read
In one paragraph

Article in Cancer medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

20 citing papers in PubMed, 38 citations in OpenAlex.

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  18. [NFAT2 mediates high glucose-induced apoptosis in glomerular podocytesNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2018
    Article
  19. Article
  20. Article
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

8 authors at 2 institutions in 1 country.

Sanrong XuDepartment of General Surgery, Affiliated Hospital of Jiangsu University, Zhenjiang, China.
Penghao ShuDepartment of Hepatobiliary Surgery, People's Hospital of Danyang, Danyang, China.
Song ZouDepartment of General Surgery, Affiliated Hospital of Jiangsu University, Zhenjiang, China.
Xiaofeng ShenDepartment of General Surgery, Affiliated Hospital of Jiangsu University, Zhenjiang, China.
Yuanqian QuDepartment of General Surgery, Affiliated Hospital of Jiangsu University, Zhenjiang, China.
Yong ZhangDepartment of General Surgery, Affiliated Hospital of Jiangsu University, Zhenjiang, China.
Kang SunDepartment of General Surgery, Affiliated Hospital of Jiangsu University, Zhenjiang, China.
Jin ZhangDepartment of General Surgery, Affiliated Hospital of Jiangsu University, Zhenjiang, China.ORCID 0000-0002-0053-9765
Jiangsu University · CNFuyang City People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nuclear factor of activated T cells (NFAT) is a family of transcription factors that have important functions in many tumors. However, the expression level and functional role of NFAT in hepatocellular carcinoma (HCC) remain unclear. In this study, we showed that NFATc1 expression was decreased in both HCC tissues and cell lines. Low expression of NFATc1 was correlated with larger tumor size, advanced tumor-node-metastasis (TNM) stage, high serum AFP level, and liver cirrhosis. Furthermore, patients with low NFATc1 expression exhibited poor prognosis. Ectopic expression of NFATc1 in HCC cells inhibited proliferation and colony formation, leading to G1 arrest and induction of apoptosis. In addition, we demonstrated that NFATc1 increased Fas ligand (FasL) expression by directly binding to its promoter and activated the extrinsic apoptotic pathway. NFATc1 and FasL expression patterns and their prognostic value for patients with HCC were also evaluated in TCGA Liver Hepatocellular Carcinoma database. Knock-down of FasL expression by siRNA in HCC cell lines abolished NFATc1's antiproliferative and pro-apoptotic effects. In conclusion, NFATc1 is frequently inactivated in HCC and functions as a tumor suppressor in liver carcinogenesis. Ectopic expression of NFATc1 in HCC cells induces apoptosis by activating the FasL-mediated extrinsic signaling pathway.

Indexed as

Signal TransductionAdultAgedApoptosisBiomarkers, TumorCarcinoma, HepatocellularCell Line, TumorFas Ligand ProteinFemaleGene Expression Regulation, NeoplasticGenes, Tumor SuppressorHumansImmunohistochemistryLiver NeoplasmsMaleMiddle AgedBiomarkers, TumorFas Ligand ProteinNFATC1 protein, humanNFATC Transcription FactorsapoptosisFas ligandhepatocellular carcinomanuclear factor of activated T-cell cytoplasmic 1tumor suppressor

Identifiers

PMID30085405
PMCPMC6143940
OpenAlexW2887370546

What Socratic holds

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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.