Evidence map›Paper›PMID 23496980›Full record

ArticleBMC cancer2013

Hypoxia induces epithelial-mesenchymal transition via activation of SNAI1 by hypoxia-inducible factor -1α in hepatocellular carcinoma.

Lin Zhang, Gang Huang, Xiaowu Li, Yujun Zhang, Yan Jiang, Junjie Shen, Jia Liu, Qingliang Wang, Jin Zhu, Xiaobin Feng and 2 more

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 181 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
181citing papers in PubMed, 2 pooled it
9.4field-weighted citation impact, top 1% 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

181 citing papers in PubMed, 2 syntheses or guidelines pooled it, 293 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Article
  5. Article
  6. The Pro-Metastatic Roles of ROS.Antioxidants (Basel, Switzerland) · 2026
    Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Non-small cell lung cancer map and analysis: exploring interconnected oncogenic signal integrators.Mammalian genome : official journal of the International Mammalian Genome Society · 2025
    Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Role ofMolecular biology research communications · 2025
    Article
  19. Mechanical signatures in cancer metastasis.npj biological physics and mechanics · 2025
    Review
  20. Article

121 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

12 authors at 2 institutions in 1 country.

Lin ZhangInstitute of Hepatobiliary Surgery, Southwest Hospital, Third Military Medical University, Chongqing, China.
Gang Huang
Xiaowu Li
Yujun Zhang
Yan Jiang
Junjie Shen
Jia Liu
Qingliang Wang
Jin Zhu
Xiaobin Feng
Jiahong Dong
Cheng Qian
Army Medical University · CNSouthwest Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundHigh invasion and metastasis are the primary factors causing poor prognosis of patients with hepatocellular carcinoma (HCC). However, the molecular mechanisms underlying these biological behaviors have not been completely elucidated. In this study, we investigate the molecular mechanism by which hypoxia promotes HCC invasion and metastasis through inducing epithelial-mesenchymal transition (EMT).

methodsThe expression of EMT markers was analyzed by immunohistochemistry. Effect of hypoxia on induction of EMT and ability of cell migration and invasion were performed. Luciferase reporter system was used for evaluation of Snail regulation by hypoxia-inducible factor -1α (HIF-1α).

resultsWe found that overexpression of HIF-1α was observed in HCC liver tissues and was related to poor prognosis of HCC patients. HIF-1α expression profile was correlated with the expression levels of SNAI1, E-cadherin, N-cadherin and Vimentin. Hypoxia was able to induce EMT and enhance ability of invasion and migration in HCC cells. The same phenomena were also observed in CoCl2-treated cells. The shRNA-mediated HIF-1α suppression abrogated CoCl2-induced EMT and reduced ability of migration and invasion in HCC cells. Luciferase assay showed that HIF-1α transcriptional regulated the expression of SNAI1 based on two hypoxia response elements (HREs) in SNAI1 promoter.

conclusionsWe demonstrated that hypoxia-stabilized HIF1α promoted EMT through increasing SNAI1 transcription in HCC cells. This data provided a potential therapeutic target for HCC treatment.

Indexed as

CadherinsCarcinoma, HepatocellularCell CycleCell Line, TumorCell MovementCobaltEpithelial-Mesenchymal TransitionGene ExpressionGene Expression Regulation, NeoplasticHumansHypoxiaHypoxia-Inducible Factor 1, alpha SubunitLiver NeoplasmsPrognosisProtein StabilitySnail Family Transcription FactorsCadherinsCobaltcobaltous chlorideHypoxia-Inducible Factor 1, alpha SubunitSNAI1 protein, humanSnail Family Transcription FactorsTranscription FactorsVimentin

Identifiers

PMID23496980
PMCPMC3614870
OpenAlexW2095510412

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.