Evidence map›Paper›PMID 26698646›Full record

ArticleHepatology (Baltimore, Md.)2016

Actin-like 6A predicts poor prognosis of hepatocellular carcinoma and promotes metastasis and epithelial-mesenchymal transition.

Shuai Xiao, Rui-Min Chang, Ming-Yang Yang, Xiong Lei, Xiao Liu, Wen-Bin Gao, Jing-Lei Xiao, Lian-Yue Yang

Open access · hybridAbstract readComparative Study
In one paragraph

Article in Hepatology (Baltimore, Md.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers.

0numbers the graph read from it
0cells of the map it votes in
78citing papers in PubMed
5.0field-weighted citation impact, top 4% 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

78 citing papers in PubMed, 159 citations in OpenAlex.

  1. Article
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  5. Current research of the Notch pathway in hepatocellular carcinoma.European journal of medical research · 2025
    Review
  6. Article
  7. Actin-Like Protein 6A as an Oncogene and Therapeutic Target in Cancer.International journal of medical sciences · 2025
    Review
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  18. Water channel protein AQP1 in cytoplasm is a critical factor in breast cancer local invasion.Journal of experimental & clinical cancer research : CR · 2023
    Article
  19. Article
  20. Article

18 more citing papers are in PubMed but not listed here.

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.

Shuai XiaoLiver Cancer Laboratory, Department of Surgery, Xiangya Hospital, Central South University, Changsha, China.
Rui-Min ChangLiver Cancer Laboratory, Department of Surgery, Xiangya Hospital, Central South University, Changsha, China.
Ming-Yang YangLiver Cancer Laboratory, Department of Surgery, Xiangya Hospital, Central South University, Changsha, China.
Xiong LeiLiver Cancer Laboratory, Department of Surgery, Xiangya Hospital, Central South University, Changsha, China.
Xiao LiuLiver Cancer Laboratory, Department of Surgery, Xiangya Hospital, Central South University, Changsha, China.
Wen-Bin GaoLiver Cancer Laboratory, Department of Surgery, Xiangya Hospital, Central South University, Changsha, China.
Jing-Lei XiaoLiver Cancer Laboratory, Department of Surgery, Xiangya Hospital, Central South University, Changsha, China.
Lian-Yue YangLiver Cancer Laboratory, Department of Surgery, Xiangya Hospital, Central South University, Changsha, China.
Central South University · CNXiangya Hospital Central South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

unlabelledHepatocellular carcinoma (HCC) is one of the most lethal cancers worldwide because of metastasis. Epithelial-mesenchymal transition (EMT) is widely considered to be crucial to the invasion-metastasis cascade during cancer progression. Actin-like 6A (ACTL6A) is initially verified important for cell proliferation, differentiation, and migration. In this study, we find that ACTL6A plays an essential role in metastasis and EMT of HCC. ACTL6A expression is up-regulated in HCC cells and tissues. A high level of ACTL6A in HCCs is correlated with aggressive clinicopathological features and is an independent poor prognostic factor for overall and disease-free survival of HCC patients. Ectopic expression of ACTL6A markedly promotes HCC cells migration, invasion, as well as EMT in vitro and promotes tumor growth and metastasis in the mouse xenograft model. Opposite results are observed when ACTL6A is knocked down. Mechanistically, ACTL6A promotes metastasis and EMT through activating Notch signaling. ACTL6A knockdown has the equal blockage effect as the Notch signaling inhibitor, N-[N-(3,5-difluorophenacetyl)-L-alanyl]-S-phenylglycine t-butylester, in HCC cells. Further studies indicate that ACTL6A might manipulate SRY (sex determining region Y)-box 2 (SOX2) expression and then activate Notch1 signaling.

conclusionsACTL6A promotes metastasis and EMT by SOX2/Notch1 signaling, indicating a prognostic biomarker candidate and a potential therapeutic target for HCC.

Indexed as

Gene Expression Regulation, NeoplasticActinsAdultAgedAnalysis of VarianceAnimalsBiopsy, NeedleCarcinoma, HepatocellularChromosomal Proteins, Non-HistoneDisease Models, AnimalDNA-Binding ProteinsEpithelial-Mesenchymal TransitionFemaleHumansImmunohistochemistryLiver NeoplasmsActinsACTL6A protein, humanChromosomal Proteins, Non-HistoneDNA-Binding Proteins

Identifiers

PMID26698646
PMCPMC4834727
OpenAlexW2270641965

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.