Evidence map›Paper›PMID 27297407›Full record

ArticleJournal of experimental & clinical cancer research : CR2016

Decreased brain-expressed X-linked 4 (BEX4) expression promotes growth of oral squamous cell carcinoma.

Wei Gao, John Zeng-Hong Li, Si-Qi Chen, Chiao-Yun Chu, Jimmy Yu-Wai Chan, Thian-Sze Wong

Open access · goldAbstract read
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.0field-weighted citation impact, top 22% 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

16 citing papers in PubMed, 27 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. FOXP2 mediates ZSCAN18 transcriptional activation to inhibit oral squamous cell carcinoma progression by blocking Hedgehog signaling.Mammalian genome : official journal of the International Mammalian Genome Society · 2025
    Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
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

6 authors at 1 institution in 1 country.

Wei GaoDepartment of Surgery, The University of Hong Kong, Hong Kong SAR, China.
John Zeng-Hong LiDepartment of Surgery, The University of Hong Kong, Hong Kong SAR, China.
Si-Qi ChenDepartment of Surgery, The University of Hong Kong, Hong Kong SAR, China.
Chiao-Yun ChuDepartment of Surgery, The University of Hong Kong, Hong Kong SAR, China.
Jimmy Yu-Wai ChanDepartment of Surgery, The University of Hong Kong, Hong Kong SAR, China.
Thian-Sze WongDepartment of Surgery, The University of Hong Kong, Hong Kong SAR, China. thainsze@gmail.com.
University of Hong Kong · HK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundBrain-expressed X-linked (BEX) 4 is a member of BEX family. The functional role of BEX4 in oral squamous cell carcinoma (OSCC) remains unknown.

methodsExpression level of BEX family members (BEX1-5) in OSCC tissues and the paired normal epithelial were examined. Functions of epigenetic changes (DNA methylation and histone modifications) on BEX4 suppression in OSCC were examined by zebularine and trichostatin A (TSA) treatment on OSCC cell lines. Lentivector containing full-length BEX4 was used to generate OSCC cell lines with stable BEX4 expression. Effects of BEX4 expression on OSCC proliferation were monitored with xCELLigence RTCA real-time cell analyzer. BEX4-overexpressing CAL27 was implanted into nude mice to evaluate the effects on tumor growth in vivo. The signaling pathways regulated by BEX4 in OSCC was explored using human whole-transcript expression microarray.

resultsAmong the 5 BEX family members, BEX1 and BEX4 showed significant down-regulation in OSCC (P < 0.001). BEX3, in comparison, was overexpressed in the primary tumor. BEX4 expression in OSCC cell lines was re-activated after zebularine and TSA treatment. High BEX4 expression could suppress proliferation of OSCC in vitro. Subcutaneous tumor volume of BEX4-overexpressing CAL27 was remarkably reduced in nude mice. Microarray experiment showed that S100A family members (S100A7, S100A7A, S100A8, S100A9 & S100A12) might be the downstream targets of BEX4 in OSCC.

conclusionsBEX4 functions as tumor suppressor by inhibiting proliferation and growth of oral cancer. Decreased BEX4 contributes to the increased proliferative propensity of OSCC.

Indexed as

Down-RegulationAnimalsCarcinoma, Squamous CellCell Line, TumorCell ProliferationEpigenesis, GeneticFemaleGene Expression ProfilingGene Expression Regulation, NeoplasticHumansMaleMiceMice, NudeMicrotubule-Associated ProteinsMouth NeoplasmsNeoplasm TransplantationBEX4 protein, humanMicrotubule-Associated ProteinsOncogene ProteinsS100 ProteinsBEX4Brain-expressed X-linked familyOral cancerS100A familySquamous cell carcinomaTumor growth

Identifiers

PMID27297407
PMCPMC4906687
OpenAlexW2437028154

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.