Evidence map›Paper›PMID 25909165›Full record

ArticleOncotarget2015

Flotillin-2 promotes nasopharyngeal carcinoma metastasis and is necessary for the epithelial-mesenchymal transition induced by transforming growth factor-β.

Liang Zhao, Li Lin, Changqie Pan, Min Shi, Yulin Liao, Jianping Bin, Wangjun Liao

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
3.8field-weighted citation impact, top 7% 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

31 citing papers in PubMed, 44 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Observational
  9. Article
  10. Article
  11. Flotillin membrane domains in cancer.Cancer metastasis reviews · 2020
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. 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

7 authors at 2 institutions in 1 country.

Liang ZhaoDepartment of Oncology, Nanfang Hospital, Southern Medical University, Guangzhou Guangdong 510515, China.
Li LinDepartment of Oncology, Nanfang Hospital, Southern Medical University, Guangzhou Guangdong 510515, China.
Changqie PanDepartment of Oncology, Nanfang Hospital, Southern Medical University, Guangzhou Guangdong 510515, China.
Min ShiDepartment of Oncology, Nanfang Hospital, Southern Medical University, Guangzhou Guangdong 510515, China.
Yulin LiaoDepartment of Cardiology, Nanfang Hospital, Southern Medical University, Guangzhou Guangdong 510515, China.
Jianping BinDepartment of Cardiology, Nanfang Hospital, Southern Medical University, Guangzhou Guangdong 510515, China.
Wangjun LiaoDepartment of Oncology, Nanfang Hospital, Southern Medical University, Guangzhou Guangdong 510515, China.
Southern Medical University · CNNanfang Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Transforming growth factor-β (TGF-β) promotes cancer metastasis via the epithelial-mesenchymal transition (EMT) but the underlying mechanisms in nasopharyngeal carcinoma (NPC) remain unclear. Flotillin-2 (Flot2), a specialized lipid raft domain in cellular membrane, was reported to promote cancer metastasis. Recently, in neuropathy, it was also suggested that Flot2 was involved in Src activation, which is known as the downstream signal of TGF-β. Therefore, we intended to find out the relationship between Flot2 and TGF-β in the process of nasopharyngeal carcinoma (NPC) metastasis. In this study, we found that Flot2 expression level positively correlated with the cancer stage in NPC tissues. Elevated Flot2 in tumor tissue was an independent prognostic marker, and higher Flot2 expression level showed shorter overall survival time in 181 NPC patients. In NPC cells, silencing Flot2 reversed the metastatic effect induced by TGF-β. Moreover, TGF-β-induced Src phosphorylation was significantly inhibited by Flot2 knocking down. As the consequence of Flot2 inhibition, the expression of the epithelial biomarker E-cadherin was upregulated, while the mesenchymal marker vimentin and signaling transducer β-catenin was suppressed. In conclusions, Flot2 is an indispensable member for TGF-β signaling, which is essential for the EMT process in NPC metastasis. Suppressing Flot2 may be a novel way against TGF-β-induced EMT.

Indexed as

Epithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticAgedAntigens, CDBiomarkersCadherinsCarcinomaCell Line, TumorFemaleHumansMaleMembrane MicrodomainsMembrane ProteinsMiddle AgedMultivariate AnalysisNasopharyngeal CarcinomaAntigens, CDBiomarkersCadherinsCDH1 protein, humanflotillinsMembrane ProteinsTransforming Growth Factor beta1epithelial-mesenchymal transitionFlotillin-2metastasisnasopharyngeal carcinomatransforming growth factor-β

Identifiers

PMID25909165
PMCPMC4496397
OpenAlexW1570706727

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.