Evidence map›Paper›PMID 29137415›Full record

ArticleOncotarget2017

Ubiquitin conjugating enzyme E2 L3 promoted tumor growth of NSCLC through accelerating p27kip1 ubiquitination and degradation.

Xingjie Ma, Junjie Zhao, Fan Yang, Haitao Liu, Weibo Qi

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.0field-weighted citation impact, top 24% 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

15 citing papers in PubMed, 21 citations in OpenAlex.

  1. Ubiquitin-conjugating Enzymes in Cancer.International journal of biological sciences · 2026
    Review
  2. International journal of biological sciences · 2026
    Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Review
  11. Review
  12. Article
  13. Article
  14. Stabilization of p27FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019
    Article
  15. 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

5 authors at 2 institutions in 1 country.

Xingjie MaDepartment of Cardiothoracic Surgery, The First Affiliated Hospital of Jiaxing University, Jiaxing, Zhejiang, China.
Junjie ZhaoDepartment of Cardiothoracic Surgery, The First Affiliated Hospital of Jiaxing University, Jiaxing, Zhejiang, China.
Fan YangDepartment of Cardiothoracic Surgery, The First Affiliated Hospital of Jiaxing University, Jiaxing, Zhejiang, China.
Haitao LiuDepartment of Cardiothoracic Surgery, The First Affiliated Hospital of Jiaxing University, Jiaxing, Zhejiang, China.
Weibo QiDepartment of Cardiothoracic Surgery, The First Affiliated Hospital of Jiaxing University, Jiaxing, Zhejiang, China.
Jiaxing University · CNFirst Hospital of Jiaxing · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The molecular pathogenesis of human lung cancer has not been completely clarified. Here, we reported that UBE2L3, a member of the ubiquitin-conjugating enzymes (E2s), were overexpressed in non-small-cell lung cancer (NSCLC) tissues compared with the non-tumor tissues. High expression of UBE2L3 was correlated with advanced tumor stage and adverse outcomes. Knockdown of UBE2L3 inhibited NSCLC cell growth while ectopic expression of UBE2L3 promoted NSCLC cell growth in a cell cycle dependent manner. The results of subcutaneous tumor xenograft studies revealed that knockdown of UBE2L3 attenuated the

Indexed as

degradationNSCLCp27kip1UBE2L3ubiquitination

Identifiers

PMID29137415
PMCPMC5663587
OpenAlexW2747686738

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.