Evidence map›Paper›PMID 23812429›Full record

ArticleOncogene2014

As an independent prognostic factor, FAT10 promotes hepatitis B virus-related hepatocellular carcinoma progression via Akt/GSK3β pathway.

L Liu, Z Dong, J Liang, C Cao, J Sun, Y Ding, D Wu

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed, 1 pooled it
4.0field-weighted citation impact, top 5% 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

41 citing papers in PubMed, 1 synthesis or guideline pooled it, 72 citations in OpenAlex.

  1. Pooled it
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  6. FAT10 induces immune suppression by upregulating PD-L1 expression in hepatocellular carcinoma.Apoptosis : an international journal on programmed cell death · 2024
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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

7 authors at 2 institutions in 1 country.

L LiuHepatology Unit and Department of Infectious Diseases, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Z DongDepartment of Radiation Oncology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
J LiangDepartment of Radiation Oncology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
C CaoDepartment of Radiation Oncology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
J SunDepartment of Radiation Oncology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Y Ding1] Hepatology Unit and Department of Infectious Diseases, Nanfang Hospital, Southern Medical University, Guangzhou, China [2] Department of Radiation Oncology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
D WuDepartment of Radiation Oncology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Nanfang Hospital · CNSouthern Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

FAT10 is an oncogene that is localized at 6q21.3, a region frequently amplified in hepatocellular carcinoma (HCC). Recently, growing attention has been paid to its effect in the initiation of various cancers. However, there has been little research into the influence of FAT10 on the progression and prognosis of HCC, especially in hepatitis B virus (HBV)-related HCC. Here, we aimed at investigating clincopathological significance of FAT10 in HBV-related HCC and its underlying mechanisms. Based on the analysis of FAT10 expression in a reliable and large number of cases with 5-year follow-up, we showed that FAT10 was significantly increased in 260 samples from HBV-related HCC patients, compared with 30 normal tissue, 50 cirrhosis and matched adjacent nontumor tissues. FAT10 expression is correlated with recurrence and poor prognosis in HBV-related HCC. In addition, ectopic expression of FAT10 enhanced cell proliferation, inhibited apoptosis and induced cell cycle progression, whereas silencing FAT10 expression suppressed cell proliferation and induced apoptosis. FAT10 also induced the epithelial-mesenchymal transition (EMT) and promoted invasion of HCC cells. Furthermore, we found Akt/GSK3β pathway contributed to the effects of FAT10 in HCC cells. Blocking the Akt pathway significantly inhibited the actions of FAT10. Taken together, the ubiquitin-like protein FAT10 has a central role in regulating diverse aspects of the pathogenesis of HCC, indicating that it might be a potential therapeutic target.

Indexed as

ApoptosisCarcinoma, HepatocellularCell CycleCell ProliferationEpithelial-Mesenchymal TransitionFemaleGene ExpressionGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaHepatitis B, ChronicHumansKaplan-Meier EstimateLiver NeoplasmsMaleMiddle AgedMultivariate AnalysisGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaGSK3B protein, humanProto-Oncogene Proteins c-aktUBD protein, humanUbiquitins

Identifiers

PMID23812429
OpenAlexW2052210088

What OpenQuestion holds

Textmetadata
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.