Evidence map›Paper›PMID 24114327›Full record

ArticleCellular oncology (Dordrecht, Netherlands)2013

Interleukin-32β stimulates migration of MDA-MB-231 and MCF-7cells via the VEGF-STAT3 signaling pathway.

Jeong Su Park, Su Yun Choi, Jeong-Hyung Lee, Maria Lee, Eun Sook Nam, Ae Lee Jeong, Sunyi Lee, Sora Han, Myeong-Sok Lee, Jong-Seok Lim and 3 more

Abstract read
In one paragraph

Article in Cellular oncology (Dordrecht, Netherlands), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

35 citing papers in PubMed, 59 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Association between interleukin-32 polymorphisms and ovarian cancer in the Chinese Han population.International journal of clinical and experimental pathology · 2020
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  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 1 country.

Jeong Su ParkResearch Center for Women's Disease, Sookmyung Women's University, Seoul, 140-742, South Korea.
Su Yun Choi
Jeong-Hyung Lee
Maria Lee
Eun Sook Nam
Ae Lee Jeong
Sunyi Lee
Sora Han
Myeong-Sok Lee
Jong-Seok Lim
Do Young Yoon
Yongil Kwon
Young Yang
Sookmyung Women's University · KRHallym University · KRHallym University Medical Center · KRKangwon National University · KRKonkuk University Medical Center · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIL-32 is known to play an important role in inflammatory and autoimmune disease responses. In addition to its role in these responses, IL-32 and its different isoforms have in recent years been implicated in the development of various cancers. As of yet, the role of IL-32 in breast cancer has remained largely unknown.

resultsBy performing immunohistochemical assays on primary breast cancer samples, we found that the level of IL-32β expression was positively correlated with tumor size, number of lymph node metastases and tumor stage. In addition, we found that breast cancer-derived MDA-MB-231 cells exogenously expressing IL-32β exhibited increased migration and invasion capacities. These increased capacities were found to be associated with an increased expression of the epithelial mesenchymal transition (EMT) markers vimentin and Slug, the latter of which is responsible for the increase in vimentin transcription. To next investigate whether IL-32β enhances migration and invasion through a soluble factor, we determined the levels of several migration-stimulating ligands, and found that the production of VEGF was increased by IL-32β. In addition, we found that IL-32β-induced VEGF increased migration and invasion through STAT3 activation.

conclusionThe IL-32β-VEGF-STAT3 pathway represents an additional pathway that mediates the migration and invasion of breast cancer cells under the conditions of normoxia and hypoxia.

Indexed as

Signal TransductionBreast NeoplasmsCell HypoxiaCell Line, TumorCell MovementCell ProliferationCells, CulturedGene Expression Regulation, NeoplasticHumansImmunoblottingImmunohistochemistryInterleukinsLymphatic MetastasisMCF-7 CellsNeoplasm StagingProtein IsoformsIL32 protein, humanInterleukinsProtein IsoformsSTAT3 protein, humanSTAT3 Transcription FactorVascular Endothelial Growth Factor A

Identifiers

PMID24114327
PMCPMC13007480
OpenAlexW2094749598

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.