Evidence map›Paper›PMID 37328464›Full record

ArticleCell death & disease2023

TOPK promotes the growth of esophageal cancer in vitro and in vivo by enhancing YB1/eEF1A1 signal pathway.

Wenjie Wu, Jialuo Xu, Dan Gao, Zhenliang Xie, Wenjing Chen, Wenjing Li, Qiang Yuan, Lina Duan, Yuhan Zhang, Xiaoxiao Yang and 4 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2023. 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
2.3field-weighted citation impact, top 12% 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, 15 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. FBXW11 inhibits tumorigenesis by ubiquitinating YB1 in hepatocarcinoma.Journal of cancer research and clinical oncology · 2025
    Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. YB1 and its role in osteosarcoma: a review.Frontiers in oncology · 2024
    Review
  12. Review
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

14 authors at 1 institution in 1 country.

Wenjie Wu *Pathophysiology Department, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, 450001, China.
Jialuo Xu *Pathophysiology Department, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, 450001, China.
Dan GaoPathophysiology Department, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, 450001, China.
Zhenliang XiePathophysiology Department, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, 450001, China.
Wenjing ChenPathophysiology Department, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, 450001, China.
Wenjing LiPathophysiology Department, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, 450001, China.
Qiang YuanPathophysiology Department, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, 450001, China.
Lina DuanPathophysiology Department, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, 450001, China.
Yuhan ZhangPathophysiology Department, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, 450001, China.
Xiaoxiao YangPathophysiology Department, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, 450001, China.
Yingying ChenPathophysiology Department, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, 450001, China.
Ziming DongPathophysiology Department, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, 450001, China.
Kangdong LiuPathophysiology Department, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, 450001, China. kdliu@zzu.edu.cn.ORCID 0000-0002-4425-5625
Yanan JiangPathophysiology Department, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, 450001, China. yananjiang@zzu.edu.cn.ORCID 0000-0001-6129-643X
Zhengzhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

T-LAK-originated protein kinase (TOPK), a dual specificity serine/threonine kinase, is up-regulated and related to poor prognosis in many types of cancers. Y-box binding protein 1 (YB1) is a DNA/RNA binding protein and serves important roles in multiple cellular processes. Here, we reported that TOPK and YB1 were both highly expressed in esophageal cancer (EC) and correlated with poor prognosis. TOPK knockout effectively suppressed EC cell proliferation and these effects were reversible by rescuing YB1 expression. Notably, TOPK phosphorylated YB1 at Thr 89 (T89) and Ser 209 (S209) amino acid residues, then the phosphorylated YB1 bound with the promoter of the eukaryotic translation elongation factor 1 alpha 1 (eEF1A1) to activate its transcription. Consequently, the AKT/mTOR signal pathway was activated by up-regulated eEF1A1 protein. Importantly, TOPK inhibitor HI-TOPK-032 suppressed the EC cell proliferation and tumor growth by TOPK/YB1/eEF1A1 signal pathway in vitro and in vivo. Taken together, our study reveals that TOPK and YB1 are essential for the growth of EC, and TOPK inhibitors may be applied to retard cell proliferation in EC. This study highlights the promising therapeutic potential of TOPK as a target for treatment of EC.

Indexed as

Esophageal NeoplasmsMitogen-Activated Protein Kinase KinasesCell Line, TumorCell ProliferationHumansPeptide Elongation Factor 1Signal TransductionMitogen-Activated Protein Kinase KinasesPDZ-binding kinasePeptide Elongation Factor 1

Identifiers

PMID37328464
PMCPMC10276051
OpenAlexW4380992174

What Socratic 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 Socratic graph.