Evidence map›Paper›PMID 31019204›Full record

ArticleCell death & disease2019

Elevation of O-GlcNAc and GFAT expression by nicotine exposure promotes epithelial-mesenchymal transition and invasion in breast cancer cells.

Nana Zhang, Tong Zhu, Kairan Yu, Meiyun Shi, Xue Wang, Lingyan Wang, Tianmiao Huang, Wenli Li, Yubo Liu, Jianing Zhang

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

17 citing papers in PubMed, 32 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Review
  17. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 2 institutions in 1 country.

Nana ZhangSchool of Life Science & Medicine, Dalian University of Technology, Panjin, China.
Tong ZhuSchool of Life Science & Medicine, Dalian University of Technology, Panjin, China.
Kairan YuSchool of Life Science & Medicine, Dalian University of Technology, Panjin, China.
Meiyun ShiSchool of Life Science & Medicine, Dalian University of Technology, Panjin, China.
Xue WangSchool of Life Science & Medicine, Dalian University of Technology, Panjin, China.
Lingyan WangSchool of Life Science & Medicine, Dalian University of Technology, Panjin, China.
Tianmiao HuangSchool of Life Science & Medicine, Dalian University of Technology, Panjin, China.
Wenli LiSchool of Life Science & Medicine, Dalian University of Technology, Panjin, China.
Yubo LiuSchool of Life Science & Medicine, Dalian University of Technology, Panjin, China. liuyubo@dlut.edu.cn.
Jianing ZhangSchool of Life Science & Medicine, Dalian University of Technology, Panjin, China. jnzhang@dlut.edu.cn.
Dalian University · CNDalian University of Technology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cigarette smoking has been shown to be a carcinogenic factor in breast cancer. Nicotine (Nic), an active component of tobacco, has been found to induce epithelial-mesenchymal transition (EMT) in breast cancer cells. However, the alterations in protein O-GlcNAcylation in Nic-mediated tumorigenesis and malignization mechanisms are less well studied. Herein, we found that cellular O-GlcNAcylation dramatically increased in human breast cancer cells with EMT activation induced by Nic. Elevated O-GlcNAcylation subsequently promoted Nic-induced EMT activation and increased cell migratory abbility. In addition, we demonstrated that a differentiation factor for the mammary epithelium, CCAAT/enhancer-binding protein B (CEBPB), was involved in Nic-induced hyper-O-GlcNAcylation via transcriptional regulation of the expression of the key enzyme glutamine: fructose-6-phosphate amidotransferase (GFAT) and thus increased the flux through the hexosamine biosynthetic pathway (HBP). Finally, elevated O-GlcNAcylation of the transcriptional repressor C/EBP homologous protein (CHOP) suppressed its heterodimerization with CEBPB and facilitated the DNA-binding activity of CEBPB, further generating positive feedback that enhanced EMT upon Nic stimulation. In conclusion, our results have revealed a new regulatory mechanism involving CEBPB/GFAT-induced hyper-O-GlcNAcylation that plays a key role in EMT and smoking-mediated breast cancer progression.

Indexed as

AcylationBreast NeoplasmsCCAAT-Enhancer-Binding Protein-betaCell Line, TumorCell MovementEpithelial-Mesenchymal TransitionFemaleGlutamine-Fructose-6-Phosphate Transaminase (Isomerizing)HumansN-AcetylglucosaminyltransferasesNicotinePromoter Regions, GeneticRNA InterferenceRNA, Small InterferingTranscription Factor CHOPCCAAT-Enhancer-Binding Protein-betaCEBPB protein, humanDDIT3 protein, humanGlutamine-Fructose-6-Phosphate Transaminase (Isomerizing)N-AcetylglucosaminyltransferasesNicotineO-GlcNAc transferaseRNA, Small InterferingTranscription Factor CHOP

Identifiers

PMID31019204
PMCPMC6482138
OpenAlexW2940903189

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.