Evidence map›Paper›PMID 24778926›Full record

ReviewJAK-STAT2014

The involvement of JAK-STAT3 in cell motility, invasion, and metastasis.

Yong Teng, James L Ross, John K Cowell

Open access · bronzeAbstract readReview
In one paragraph

Review in JAK-STAT, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 95 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
95citing papers in PubMed, 1 pooled it
5.2field-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

95 citing papers in PubMed, 1 synthesis or guideline pooled it, 153 citations in OpenAlex.

  1. Pooled it
  2. Review
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  12. Importance of STAT3 signaling in preeclampsia (Review).International journal of molecular medicine · 2025
    Review
  13. Article
  14. Review
  15. Review
  16. Discovery of a 6-Aminobenzo[ACS pharmacology & translational science · 2024
    Article
  17. Article
  18. Article
  19. Article
  20. Article

35 more citing papers are in PubMed but not listed here.

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

3 authors at 2 institutions in 1 country.

Yong TengGeorgia Regents University Cancer Center; Augusta, GA USA.
James L RossGeorgia Regents University Cancer Center; Augusta, GA USA.
John K CowellGeorgia Regents University Cancer Center; Augusta, GA USA.
Augusta University · USGeorgia Regents Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

JAK-STAT3 signaling, while regulating many aspects of cancer development and progression, promotes invasion and metastasis through activation of key metastasis promoting genes such as WASF3. STAT3 promotes WASF3 expression and JAK2 independently activates it, which is required for invasion. JAK-STAT3 signaling is dependent on WASF3 function, since its inactivation in cells expressing JAK-STAT3 suppresses invasion. WASF3 overexpression leads to activation of NFκB and ZEB1 which also promote invasion through regulation of target genes involved in metastasis. NFκB frequently cooperates with STAT3 to upregulate metastasis promoting genes such as matrix metalloproteinases and cytokines, as well as to suppress microRNAs which can suppresses invasion. This better understanding of the complex role played by JAK-STAT3 in the regulation of cell movement, invasion, and metastasis provides opportunities to suppress this lethal aspect of cancer progression by not only targeting the JAK and STAT3 proteins directly, but also some of the downstream effectors of JAK-STAT3 signaling.

Indexed as

cancerinvasionJAK2metastasismotilitySTAT3WASF3

Identifiers

PMID24778926
PMCPMC3995737
OpenAlexW2042520699

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.