Evidence map›Paper›PMID 23393140›Full record

ArticleThe Journal of biological chemistry2013

Interaction with cyclin H/cyclin-dependent kinase 7 (CCNH/CDK7) stabilizes C-terminal binding protein 2 (CtBP2) and promotes cancer cell migration.

Yuchan Wang, Fang Liu, Feng Mao, Qinlei Hang, Xiaodong Huang, Song He, Yingying Wang, Chun Cheng, Huijie Wang, Guangfei Xu and 2 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
6.4field-weighted citation impact, top 3% 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

32 citing papers in PubMed, 77 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Cyclin H Regulates Lung Cancer Progression as a Carcinoma Inducer.Computational and mathematical methods in medicine · 2021
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Gastric cancer biomarkers; A systems biology approach.Biochemistry and biophysics reports · 2018
    Article
  14. Article
  15. Article
  16. IGFBP6 Regulates Cell Apoptosis and Migration in Glioma.Cellular and molecular neurobiology · 2017
    Article
  17. Article
  18. Review
  19. PKC iota promotes cellular proliferation by accelerated G1/S transition via interaction with CDK7 in esophageal squamous cell carcinoma.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
  20. Overexpression of MYCN promotes proliferation of non-small cell lung cancer.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    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

12 authors at 3 institutions in 1 country.

Yuchan WangDepartment of Pathogen and Immunology, Medical College, Nantong University, Nantong 226001, China.
Fang Liu
Feng Mao
Qinlei Hang
Xiaodong Huang
Song He
Yingying Wang
Chun Cheng
Huijie Wang
Guangfei Xu
Tianyi Zhang
Aiguo Shen
Nantong University · CNAffiliated Hospital of Nantong University · CNShanghai Medical College of Fudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

CtBP2 has been demonstrated to possess tumor-promoting capacities by virtue of up-regulating epithelial-mesenchymal transition (EMT) and down-regulating apoptosis in cancer cells. As a result, cellular CtBP2 levels are considered a key factor determining the outcome of oncogenic transformation. How pro-tumorigenic and anti-tumorigenic factors compete for fine-tuning CtBP2 levels is incompletely understood. Here we report that the cyclin H/cyclin-dependent kinase 7 (CCNH/CDK7) complex interacted with CtBP2 in vivo and in vitro. Depletion of either CCNH or CDK7 decreased CtBP2 protein levels by accelerating proteasome-dependent CtBP2 clearance. Further analysis revealed that CCNH/CDK7 competed with the tumor repressor HIPK2 for CtBP2 binding and consequently inhibited phosphorylation and dimerization of CtBP2. Phosphorylation-defective CtBP2 interacted more strongly with CCNH/CDK7 and was more resistant to degradation. Finally, overexpression of CtBP2 increased whereas depletion of CtBP2 dampened the invasive and migratory potential of breast cancer cells. CtBP2 promoted the invasion and migration of breast cancer cells in a CCNH-dependent manner. Taken together, our data have delineated a novel pathway that regulates CtBP2 stability, suggesting that targeting the CCNH/CDK7-CtBP2 axis may yield a viable anti-tumor strategy.

Indexed as

Gene Expression Regulation, NeoplasticAlcohol OxidoreductasesCell Line, TumorCell MovementCo-Repressor ProteinsCyclin-Dependent Kinase-Activating KinaseCyclin-Dependent KinasesCycloheximideHEK293 CellsHumansNeoplasm MetastasisNeoplasmsNerve Tissue ProteinsProteasome Endopeptidase ComplexProtein BindingProtein Interaction MappingAlcohol OxidoreductasesCDK7 protein, humanCo-Repressor ProteinsCTBP2 protein, humanCyclin-Dependent Kinase-Activating KinaseCyclin-Dependent KinasesCycloheximideNerve Tissue ProteinsProteasome Endopeptidase ComplexProtein Synthesis Inhibitors

Identifiers

PMID23393140
PMCPMC3610975
OpenAlexW2038162228

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.