Evidence map›Paper›PMID 24390615›Full record

ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2014

CEP55 contributes to human gastric carcinoma by regulating cell proliferation.

Jinqiu Tao, Xiaofei Zhi, Yuan Tian, Zheng Li, Yi Zhu, Weizhi Wang, Kunling Xie, Jie Tang, Xiaoyu Zhang, Linjun Wang and 1 more

Abstract read
PubMed Publisher
In one paragraph

Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

48 citing papers in PubMed, 82 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. CEP55 promotes epithelial-mesenchymal transition in renal cell carcinoma through PI3K/AKT/mTOR pathway.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2019
    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

11 authors at 2 institutions in 1 country.

Jinqiu TaoDivision of Gastric Surgery, Department of General Surgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, 210029, China.
Xiaofei Zhi
Yuan Tian
Zheng Li
Yi Zhu
Weizhi Wang
Kunling Xie
Jie Tang
Xiaoyu Zhang
Linjun Wang
Zekuan Xu
Jiangsu Province Hospital · CNNanjing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Centrosomal protein 55 (CEP55) is the latest found member in the centrosomal relative protein family, which participates in cell-cycle regulation. CEP55 exists in many kinds of normal tissues and tumour cells such as hepatocellular carcinoma, and is important in carcinogenesis. However, the role of CEP55 in the pathogenesis of gastric cancer (GC) remains unclear. The mRNA levels of CEP55 in GC tissues and GC cell lines were examined by quantitative real-time PCR, and the protein expression of CEP55 in GC tissues was detected by Western blot and immunohistochemistry. The role of CEP55 in regulating the proliferation of GC cell lines was investigated both in vitro and in vivo. CEP55 was strongly upregulated in human GC, indicating that CEP55 contributed to carcinogenesis and progression of GC. Ectopic overexpression of CEP55 enhanced the cell proliferation, colony formation, and tumourigenicity of GC cells, whereas CEP55 knockdown inhibited these effects. We discovered that cell transformation induced by CEP55 was mediated by the AKT signalling pathway. Overexpression of CEP55 enhanced the phosphorylation of AKT and inhibited the activity of p21 WAF1/Cip1. In addition, cellular proliferation was suppressed as a result of cell cycle arrest at the G2/M phase in CEP55-knockdown cells. CEP55 expression was elevated in GC compared with normal control tissues. Credible evidence showed that CEP55 can be a potential therapeutic target in GC.

Indexed as

Cell ProliferationAdultAgedAnimalsCell Cycle CheckpointsCell Cycle ProteinsCell Line, TumorCyclin-Dependent Kinase Inhibitor p21FemaleHumansMaleMiceMiddle AgedNuclear ProteinsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktCDKN1A protein, humanCell Cycle ProteinsCep55 protein, humanCyclin-Dependent Kinase Inhibitor p21Nuclear ProteinsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-akt

Identifiers

PMID24390615
OpenAlexW2074403409

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.