Evidence map›Paper›PMID 27448302›Full record

ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2016

4.1N is involved in a flotillin-1/β-catenin/Wnt pathway and suppresses cell proliferation and migration in non-small cell lung cancer cell lines.

Qin Yang, Min Zhu, Zi Wang, Hui Li, Weihua Zhou, Xiaojuan Xiao, Bin Zhang, Weixin Hu, Jing Liu

Abstract read
PubMed Publisher
In one paragraph

Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.6field-weighted citation impact, top 31% 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

11 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Tumor Suppressor 4.1N/Frontiers in genetics · 2022
    Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. 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

9 authors at 1 institution in 1 country.

Qin YangState Key Laboratory of Medical Genetics & School of Life Sciences, Central South University, 110 Xiangya Road, Changsha, 410078, China.
Min ZhuState Key Laboratory of Medical Genetics & School of Life Sciences, Central South University, 110 Xiangya Road, Changsha, 410078, China. zhumin0678@yahoo.com.
Zi WangState Key Laboratory of Medical Genetics & School of Life Sciences, Central South University, 110 Xiangya Road, Changsha, 410078, China.
Hui LiState Key Laboratory of Medical Genetics & School of Life Sciences, Central South University, 110 Xiangya Road, Changsha, 410078, China.
Weihua ZhouState Key Laboratory of Medical Genetics & School of Life Sciences, Central South University, 110 Xiangya Road, Changsha, 410078, China.
Xiaojuan XiaoState Key Laboratory of Medical Genetics & School of Life Sciences, Central South University, 110 Xiangya Road, Changsha, 410078, China.
Bin ZhangDepartment of pathology, Central South University, 110 Xiangya Road, Changsha, 410078, China.
Weixin HuState Key Laboratory of Medical Genetics & School of Life Sciences, Central South University, 110 Xiangya Road, Changsha, 410078, China.
Jing LiuState Key Laboratory of Medical Genetics & School of Life Sciences, Central South University, 110 Xiangya Road, Changsha, 410078, China.
Central South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The membrane-cytoskeletal protein 4.1N has recently been proposed as a tumor suppressor in a number of cancers of epithelial origin, including non-small-cell lung cancer (NSCLC). However, the molecular mechanism associated with 4.1N tumor suppression remains has not been thoroughly characterized. In this study, 4.1N was shown to directly interact with the lipid raft marker flotillin-1 through its FERM and U2 domains in several different NSCLC cell lines using immunoprecipitation, co-immunoprecipitation and pull-down assays. Moreover, 4.1N silencing/overexpression experiments in paired 95C/95D cells that are of homologous origin but varying endogenous 4.1N expression (high expression in 95C cells, low expression in 95D cells) indicated that 4.1N is involved in the suppression of cell proliferation and migration through a flotillin-1/β-catenin/Wnt pathway. Taken together, the findings of this study help to elucidate the novel tumor suppressor role of 4.1N in NSCLC.

Indexed as

Amino Acid Sequencebeta CateninBlotting, WesternCarcinoma, Non-Small-Cell LungCell MovementCell ProliferationCytoskeletal ProteinsGene Expression Regulation, NeoplasticHumansLung NeoplasmsMembrane ProteinsNeuropeptidesProtein BindingReverse Transcriptase Polymerase Chain ReactionRNA InterferenceWnt Signaling Pathwaybeta CateninCytoskeletal Proteinserythrocyte membrane protein band 4.1-like 1flotillinsMembrane ProteinsNeuropeptides4.1N, non-small cell lung cancer (NSCLC)Flotillin-1Flotillin-1/β-catenin/Wnt pathway

Identifiers

PMID27448302
OpenAlexW2503881822

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.