Evidence map›Paper›PMID 21540330›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2011

Cysteine-rich intestinal protein 2 (CRIP2) acts as a repressor of NF-kappaB-mediated proangiogenic cytokine transcription to suppress tumorigenesis and angiogenesis.

Arthur Kwok Leung Cheung, Josephine M Y Ko, Hong Lok Lung, Kwok Wah Chan, Eric J Stanbridge, Eugene Zabarovsky, Takashi Tokino, Lisa Kashima, Toshiharu Suzuki, Dora Lai-Wan Kwong and 3 more

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

50 citing papers in PubMed, 84 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. The impact and mechanisms of CRIP2 on the biological behavior of triple-negative breast cancer cells.Translational breast cancer research : a journal focusing on translational research in breast cancer · 2025
    Article
  14. Article
  15. Review
  16. Science advances · 2024
    Article
  17. Article
  18. Article
  19. 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

13 authors at 5 institutions in 6 countries.

Arthur Kwok Leung CheungDepartment of Clinical Oncology and Center for Cancer Research, University of Hong Kong, Hong Kong, People's Republic of China.
Josephine M Y Ko
Hong Lok Lung
Kwok Wah Chan
Eric J Stanbridge
Eugene Zabarovsky
Takashi Tokino
Lisa Kashima
Toshiharu Suzuki
Dora Lai-Wan Kwong
Daniel Chua
Sai Wah Tsao
Maria Li Lung
Sapporo Medical University · JPUniversity of Hong Kong · HKHokkaido University · JPKarolinska Institutet · SEUniversity of California, Irvine · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chromosome 14 was transferred into tumorigenic nasopharyngeal carcinoma and esophageal carcinoma cell lines by a microcell-mediated chromosome transfer approach. Functional complementation of defects present in the cancer cells suppressed tumor formation. A candidate tumor-suppressor gene, cysteine-rich intestinal protein 2 (CRIP2), located in the hot spot for chromosomal loss at 14q32.3, was identified as an important candidate gene capable of functionally suppressing tumor formation. Previous studies have shown that CRIP2 is associated with development. To date, no report has provided functional evidence supporting a role for CRIP2 in tumor development. The present study provides unequivocal evidence that CRIP2 can functionally suppress tumorigenesis. CRIP2 is significantly down-regulated in nasopharyngeal carcinoma cell lines and tumors. CRIP2 reexpression functionally suppresses in vivo tumorigenesis and angiogenesis; these effects are induced by its transcription-repressor capability. It interacts with the NF-κB/p65 to inhibit its DNA-binding ability to the promoter regions of the major proangiogenesis cytokines critical for tumor progression, including IL6, IL8, and VEGF. In conclusion, we provide compelling evidence that CRIP2 acts as a transcription repressor of the NF-κB-mediated proangiogenic cytokine expression and thus functionally inhibits tumor formation and angiogenesis.

Indexed as

Transcription, GeneticAdaptor Proteins, Signal TransducingAngiogenic ProteinsCell LineCell Line, TumorCell Transformation, NeoplasticChromosomes, Human, Pair 14CytokinesHumansLIM Domain ProteinsNeovascularization, PathologicNF-kappa BRepressor ProteinsTumor Suppressor ProteinsAdaptor Proteins, Signal TransducingAngiogenic ProteinsCRIP2 protein, humanCytokinesLIM Domain ProteinsNF-kappa BRepressor ProteinsTumor Suppressor Proteins

Identifiers

PMID21540330
PMCPMC3100921
OpenAlexW1965879808

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.