Evidence map›Paper›PMID 24067369›Full record

ArticleCell cycle (Georgetown, Tex.)2013

HIC1 interacts with and modulates the activity of STAT3.

Ying-Mei Lin, Chia-Mei Wang, Jen-Chong Jeng, Dominique Leprince, Hsiu-Ming Shih

Open access · bronzeAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.9field-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

13 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Article
  6. Review
  7. STAT3 Interactors as Potential Therapeutic Targets for Cancer Treatment.International journal of molecular sciences · 2018
    Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. 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 4 institutions in 4 countries.

Ying-Mei LinInstitute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan, ROC.
Chia-Mei Wang
Jen-Chong Jeng
Dominique Leprince
Hsiu-Ming Shih
Taipei Hospital · TWInstitute of Biomedical Science · GBInstitut Pasteur de Lille · FRNational Defense Medical Center · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

HIC1 (hypermethylated in cancer 1) is a tumor suppressor gene, expression of which is frequently suppressed in human cancers. Very little is known about the molecular basis of HIC1 in antagonizing oncogenic pathways. Here, we report that HIC1 forms complexes with the signal transducers and activators of transcription 3 (STAT3) and attenuates STAT3-mediated transcription. STAT3 was identified as a HIC1-interacting protein by affinity capture and followed by mass spectrometry analysis. Overexpression or depletion of HIC1 resulted in decreased or increased levels of interleukin-6 (IL-6)/oncostatin M (OSM)-induced STAT3-mediated reporter activity and expression of target genes such as VEGF and c-Myc, respectively. Furthermore, HIC1 suppressing the VEGF and c-Myc promoter activity and the colony formation of MDA-MB 231 cells were STAT3-dependent. Further studies showed that HIC1 interacts with the DNA binding domain of STAT3 and suppresses the binding of STAT3 to its target gene promoters. Domain mapping study revealed that HIC1 C-terminal domain binds to STAT3. HIC1 mutant defective in STAT3 interaction reduced its repressive effect on STAT3 DNA binding activity, the reporter activity and gene expression of the VEGF and c-Myc genes, and cell growth in MDA-MB 231 cells. Altogether, our findings not only provide a novel role of HIC1 in antagonizing STAT3-mediated activation of VEGF and c-Myc gene expression and cell growth, but also elucidate a molecular basis underlying the inhibitory effect of HIC1 on STAT3 transcriptional potential.

Indexed as

Gene Expression Regulation, NeoplasticTranscription, GeneticAmino Acid SequenceBinding SitesCell Line, TumorGenes, ReporterHumansInterleukin-6Kruppel-Like Transcription FactorsLuciferasesMolecular Sequence DataOncostatin MPromoter Regions, GeneticProtein BindingProtein Interaction Domains and MotifsProto-Oncogene Proteins c-mycHIC1 protein, humanIL6 protein, humanInterleukin-6Kruppel-Like Transcription FactorsLuciferasesMYC protein, humanOncostatin MOSM protein, humanProto-Oncogene Proteins c-mycSTAT3 protein, humanSTAT3 Transcription FactorVascular Endothelial Growth Factor AVEGFA protein, humanDNA bindingHIC1protein interactionSTAT3transcriptional regulation

Identifiers

PMID24067369
PMCPMC3755077
OpenAlexW2079452060

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.