Evidence map›Paper›PMID 25678857›Full record

ArticleCancer cell international2015

Arf6 regulates EGF-induced internalization of E-cadherin in breast cancer cells.

Rui Xu, Yujie Zhang, Luo Gu, Jianchao Zheng, Jie Cui, Jing Dong, Jun Du

Open access · goldAbstract read
In one paragraph

Article in Cancer cell international, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

12 citing papers in PubMed, 29 citations in OpenAlex.

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  9. Downregulation of TBC1 Domain Family Member 24 (BC1D24) Inhibits Breast Carcinoma Growth via IGF1R/PI3K/AKT Pathway.Medical science monitor : international medical journal of experimental and clinical research · 2018
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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 1 institution in 1 country.

Rui XuState Key Laboratory of Reproductive Medicine, Nanjing Medical University, 140 Hanzhong Road, Nanjing, Jiangsu 210029 China ; Department of Physiology, Nanjing Medical University, Nanjing, Jiangsu 210029 China ; Department of Biotechnology, Nanjing Medical University, Nanjing, Jiangsu 210029 China.
Yujie ZhangDepartment of Physiology, Nanjing Medical University, Nanjing, Jiangsu 210029 China ; Department of Biochemistry and Molecular Biology, Nanjing Medical University, Nanjing, Jiangsu 210029 China.
Luo GuState Key Laboratory of Reproductive Medicine, Nanjing Medical University, 140 Hanzhong Road, Nanjing, Jiangsu 210029 China ; Department of Physiology, Nanjing Medical University, Nanjing, Jiangsu 210029 China.
Jianchao ZhengDepartment of Physiology, Nanjing Medical University, Nanjing, Jiangsu 210029 China.
Jie CuiDepartment of Biochemistry and Molecular Biology, Nanjing Medical University, Nanjing, Jiangsu 210029 China.
Jing DongDepartment of Biochemistry and Molecular Biology, Nanjing Medical University, Nanjing, Jiangsu 210029 China ; Department of Epidemiology and Biostatistics and Ministry of Education (MOE) Key Lab for Modern Toxicology, Nanjing Medical University, Nanjing, Jiangsu 210029 China.
Jun DuState Key Laboratory of Reproductive Medicine, Nanjing Medical University, 140 Hanzhong Road, Nanjing, Jiangsu 210029 China ; Department of Physiology, Nanjing Medical University, Nanjing, Jiangsu 210029 China.
Nanjing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

E-cadherin internalization facilitates dissolution of adherens junctions and promotes tumor cell epithelial-mesenchymal transition (EMT) and migration. Our previous results have shown that Arf6 exerts pro-migratory action in breast cancer cells after EGF stimulation. Despite the fact that EGF signaling stimulates EMT of breast cancer cells, the effect of Arf6 on internalization of E-cadherin of breast cancer cells under EGF treatment remains to be determined. Here, we showed that EGF dose-dependently stimulated E-cadherin internalization by MCF-7 cells with the maximal effect at 50 ng/ml. Meanwhile, EGF treatment markedly increased Arf6 activation. Arf6 was involved in complexes of E-cadherin, and more E-cadherin was pulled down with Arf6 when the activity of the latter was increased. Immunoblotting and immunofluorescence assays showed that transfection breast cancer cells with Arf6-T27N or Arf6 siRNA suppressed EGF-induced E-cadherin internalization. Taken together, our study demonstrated that Arf6 activation plays a potential role in EGF-induced E-cadherin internalization, providing new mechanism underlying the effect of Arf6 on promoting breast cancer cell metastasis.

Indexed as

Arf6Breast cancerE-cadherinEGFInternalization

Identifiers

PMID25678857
PMCPMC4326200
OpenAlexW2122893821

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.