Evidence map›Paper›PMID 24281831›Full record

ArticleJournal of molecular medicine (Berlin, Germany)2014

Increased expression of S100A6 promotes cell proliferation and migration in human hepatocellular carcinoma.

Ziqiang Li, Mei Tang, Bo Ling, Shiying Liu, Yu Zheng, Chunlai Nie, Zhu Yuan, Liangxue Zhou, Gang Guo, Aiping Tong and 1 more

Abstract read
PubMed Publisher
In one paragraph

Article in Journal of molecular medicine (Berlin, Germany), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

29 citing papers in PubMed, 57 citations in OpenAlex.

  1. Article
  2. Article
  3. Three-dimensional genome architecture in intrahepatic cholangiocarcinoma.Cellular oncology (Dordrecht, Netherlands) · 2025
    Article
  4. Review
  5. Article
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  8. Review
  9. Article
  10. Article
  11. S100A6 Protein-Expression and Function in Norm and Pathology.International journal of molecular sciences · 2023
    Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Observational
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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

11 authors at 2 institutions in 1 country.

Ziqiang LiState Key Laboratory of Biotherapy and Cancer Center, West China Hospital, West China Medical School, Sichuan University, Chengdu, People's Republic of China, ziqiangli21@gmail.com.
Mei Tang
Bo Ling
Shiying Liu
Yu Zheng
Chunlai Nie
Zhu Yuan
Liangxue Zhou
Gang Guo
Aiping Tong
Yuquan Wei
Sichuan University · CNState Key Laboratory of Biotherapy

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

unlabelledHigh levels of S100A6 have been associated with poor outcome in some types of human cancers, but the role of S100A6 in the molecular pathogenesis of these cancers is largely unknown. This study was performed to explore the expression and functional roles of S100A6 in hepatocellular carcinoma (HCC). The expression level of S100A6 in HCC tumor and corresponding peritumoral tissues were determined by immunohistochemistry analysis. The potential functions of S100A6 in tumorigenesis and metastasis were analyzed by cell proliferation, migration, and invasion assays in human liver cancer cells. Moreover, through expression and purification of S100A6 recombinant protein tagged with cell-penetrating peptide, we analyzed its complex extracellular/intracellular effects in a S100A6-silenced cellular model. As a result, the expression of S100A6 was up-regulated in human HCC compared with adjacent peritumoral tissues. S100A6 silencing inhibited the growth and motility of HCC cells, while intracellular re-expression of S100A6 could rescue the proliferation and migration defects. Intracellular over-expression of S100A6 resulted in down-regulation of E-cadherin expression and promoted nuclear accumulation of β-catenin. Moreover, we found that the enhanced cell proliferation and motility after S100A6 stimulation were dependent on the activation of PI3K/AKT pathway. These results suggest that S100A6 may be involved in promotion and progression of human liver cancer. KEY MESSAGES: S100A6 is overexpressed in human hepatocellular carcinoma clinical specimens. S100A6 promotes proliferation and migration of human hepatoma cells. Overexpression of S100A6 results in alteration of E-cadherin and β-catenin. The multi-effects of S100A6 may be mediated in part by PI3K/AKT pathway activation.

Indexed as

Animalsbeta CateninCadherinsCarcinogenesisCarcinoma, HepatocellularCell Cycle ProteinsCell MovementCell NucleusCell ProliferationCell ShapeCholangiocarcinomaDown-RegulationG1 Phase Cell Cycle CheckpointsGene SilencingHep G2 CellsHumansbeta CateninCadherinsCell Cycle ProteinsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktS100A6 protein, humanS100 Calcium Binding Protein A6S100 ProteinsTetracycline

Identifiers

PMID24281831
OpenAlexW2054912117

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.