Evidence map›Paper›PMID 26125229›Full record

ArticleOncotarget2015

Upregulation of FAM83D affects the proliferation and invasion of hepatocellular carcinoma.

Weijia Liao, Weilong Liu, Xing Liu, Qing Yuan, Ying Ou, Yao Qi, Wanqiu Huang, Yun Wang, Jian Huang

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

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 1 pooled it
2.3field-weighted citation impact, top 12% 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

31 citing papers in PubMed, 1 synthesis or guideline pooled it, 66 citations in OpenAlex.

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  12. Refractory alveolar rhabdomyosarcoma in an 11-year-old male.Cold Spring Harbor molecular case studies · 2021
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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

9 authors at 4 institutions in 1 country.

Weijia LiaoLaboratory of Hepatobiliary and Pancreatic Surgery, Affiliated Hospital of Guilin Medical University, Shanghai Center for Systems Biomedicine, Shanghai Jiao Tong University, Shanghai, China.
Weilong LiuShenzhen Key Laboratory of Infection and Immunity, Shenzhen Third People's Hospital, Guangdong Medical College, Shenzhen, China.
Xing LiuShanghai-MOST Key Laboratory for Disease and Health Genomics, Chinese National Human Genome Center, Shanghai, China.
Qing YuanShanghai-MOST Key Laboratory for Disease and Health Genomics, Chinese National Human Genome Center, Shanghai, China.
Ying OuShanghai-MOST Key Laboratory for Disease and Health Genomics, Chinese National Human Genome Center, Shanghai, China.
Yao QiShanghai-MOST Key Laboratory for Disease and Health Genomics, Chinese National Human Genome Center, Shanghai, China.
Wanqiu HuangTongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Yun WangShanghai-MOST Key Laboratory for Disease and Health Genomics, Chinese National Human Genome Center, Shanghai, China.
Jian HuangLaboratory of Hepatobiliary and Pancreatic Surgery, Affiliated Hospital of Guilin Medical University, Shanghai Center for Systems Biomedicine, Shanghai Jiao Tong University, Shanghai, China.
Chinese National Human Genome Center · CNGuilin Medical University · CNHuazhong University of Science and Technology · CNShenzhen Third People’s Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The identification of potential oncogenes plays an important role in finding novel therapeutic targets for many cancers, including hepatocellular carcinoma (HCC), which is one of the most common cancers worldwide. In our previous research, using microarray technology, we found that FAM83D was overexpressed in HCCs. However, whether the overexpression of FAM83D contributes to hepatocarcinogenesis remains unclear. In this study, we found that FAM83D was significantly upregulated in 76.6% (167 of 218) of the HCC specimens at the mRNA level and in 69.44% (50 of 72) of the HCC specimens at the protein level compared with adjacent non-cancerous liver specimens, as indicated by RT-PCR and immunohistochemical staining, respectively. The FAM83DmRNA expression level was positively correlated with the level of alpha-fetoprotein (AFP) (≥100 ng/ml), the clinical TNM stage, the presence of a portal vein tumor thrombus (PVTT), disease-free survival (DFS) and the overall survival (OS) time of the HCC patients (P < 0.05). Knocking down FAM83D significantly promoted the growth of Huh7 and HepG2 cells, as demonstrated in an RNA interference assay. Moreover, the DNA methylation status of the FAM83D promoter was significantly reduced in the HCC specimens with overexpression of FAM83D gene. Our data suggest that the upregulation of FAM83D, a potential oncotarget gene, may be triggered by epigenetic events and can contribute to hepatocarcinogenesis.

Indexed as

Gene Expression Regulation, NeoplasticUp-RegulationAdultalpha-FetoproteinsCarcinogenesisCarcinoma, HepatocellularCell Cycle ProteinsCell ProliferationDisease-Free SurvivalDNA MethylationEpigenesis, GeneticFemaleHep G2 CellsHumansKaplan-Meier EstimateLiveralpha-FetoproteinsCell Cycle ProteinsFAM83D protein, humanMicrotubule-Associated ProteinsRNA, MessengerFAM83Dhepatocellular carcinomamethylationoverall survivalup-regulation

Identifiers

PMID26125229
PMCPMC4695175
OpenAlexW1654255809

What OpenQuestion holds

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LicenceCC BY
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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.