Evidence map›Paper›PMID 30186750›Full record

ArticleFEBS open bio2018

Death receptor 6 promotes ovarian cancer cell migration through KIF11.

Bianhua Shi, Jiayu Bao, Yongbin Liu, Juan Shi

Open access · goldAbstract read
In one paragraph

Article in FEBS open bio, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.1field-weighted citation impact, top 26% 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

18 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Kinesin Spindle Protein (KIF11) in Mitosis and Cancer.International journal of molecular sciences · 2025
    Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. KIF11 Is a Promising Therapeutic Target for Thyroid Cancer Treatment.Computational and mathematical methods in medicine · 2022
    Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. 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

4 authors at 1 institution in 1 country.

Bianhua ShiNational Laboratory of Medical Molecular Biology Institute of Basic Medical Sciences Chinese Academy of Medical Sciences & Peking Union Medical College Beijing China.
Jiayu BaoNational Laboratory of Medical Molecular Biology Institute of Basic Medical Sciences Chinese Academy of Medical Sciences & Peking Union Medical College Beijing China.
Yongbin LiuNational Laboratory of Medical Molecular Biology Institute of Basic Medical Sciences Chinese Academy of Medical Sciences & Peking Union Medical College Beijing China.
Juan ShiNational Laboratory of Medical Molecular Biology Institute of Basic Medical Sciences Chinese Academy of Medical Sciences & Peking Union Medical College Beijing China.
Chinese Academy of Medical Sciences & Peking Union Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The expression of death receptor 6 (DR6) is abnormal in some cancer types, but the function and underlying molecular mechanisms of DR6 in tumor progression are not yet clear. In the present study, our analysis of ovarian cancer RNA sequencing data from The Cancer Genome Atlas revealed that DR6 is upregulated in human ovarian cancer. We confirmed that the expression level of DR6 is upregulated in ovarian cancer tissues when compared with matched adjacent normal tissues. In addition, DR6 enhanced ovarian carcinoma cell migration ability, and decreased expression of DR6 inhibited the expression of matrix metalloprotease (MMP) 2 and MMP9, and increased the expression of E-cadherin. Additionally, DR6 shRNA caused a significant decrease in phosphoinositide-3-kinase (PI3K), phospho (p) -AKT, p-extracellular signal-regulated kinase (ERK), and p-mitogen-activated protein kinase kinase expression in SKOV3 cells. These results suggested that DR6 can enhance ovarian carcinoma cell migration ability through the mitogen-activated protein kinase/ERK and PI3K/AKT pathways. Notably, mass spectrometric analysis indicated that DR6 co-purified with kinesin family member 11 (KIF11), and we verified the interaction between KIF11 and DR6 by co-immunoprecipitation and glutathione

Indexed as

death receptor 6DR6KIF11migrationovarian cancerTRAF4

Identifiers

PMID30186750
PMCPMC6120224
OpenAlexW2884348708

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.