Evidence map›Paper›PMID 41374981›Full record

ArticleCancers2025

Chronic IL-1 Exposure Attenuates RELA- and STAT3-Dependent Synergistic Cytokine Signaling in Prostate Cancer Cell Lines.

Stephanie Akemi Yamauchi, Haley Dahl-Wilkie, Mohamed Hussien Mohamed Zaky, Vivian Liu, Adora Onuogu, Ahmed Abdi, Shreya Billa, Rahael Javaid, Sheza Siddiqui, Chisom Mbah and 5 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cancers, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
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

3 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
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

15 authors.

Stephanie Akemi YamauchiBiological Sciences Department, The University of Texas at Dallas, Richardson, TX 75080, USA.
Haley Dahl-WilkieBiological Sciences Department, The University of Texas at Dallas, Richardson, TX 75080, USA.
Mohamed Hussien Mohamed ZakyBiological Sciences Department, The University of Texas at Dallas, Richardson, TX 75080, USA.ORCID 0009-0003-4166-9376
Vivian LiuBiological Sciences Department, The University of Texas at Dallas, Richardson, TX 75080, USA.
Adora OnuoguBiological Sciences Department, The University of Texas at Dallas, Richardson, TX 75080, USA.
Ahmed AbdiBiological Sciences Department, The University of Texas at Dallas, Richardson, TX 75080, USA.
Shreya BillaBiological Sciences Department, The University of Texas at Dallas, Richardson, TX 75080, USA.ORCID 0009-0005-2277-3797
Rahael JavaidBiological Sciences Department, The University of Texas at Dallas, Richardson, TX 75080, USA.
Sheza SiddiquiBiological Sciences Department, The University of Texas at Dallas, Richardson, TX 75080, USA.
Chisom MbahBiological Sciences Department, The University of Texas at Dallas, Richardson, TX 75080, USA.
Olaoluwapo BankoleBiological Sciences Department, The University of Texas at Dallas, Richardson, TX 75080, USA.
Sarah WellsBiological Sciences Department, The University of Texas at Dallas, Richardson, TX 75080, USA.
Sydney GreeneBiological Sciences Department, The University of Texas at Dallas, Richardson, TX 75080, USA.
Rafah FalahBiological Sciences Department, The University of Texas at Dallas, Richardson, TX 75080, USA.
Nikki Ayanna DelkBiological Sciences Department, The University of Texas at Dallas, Richardson, TX 75080, USA.ORCID 0000-0001-9482-3830

Funding

American Cancer Society RSG-20-138-01-TBE
6 · The paper itself

Abstract

BACKGROUND/

objectivesThe milieu of inflammatory cytokines present in the prostate cancer (PCa) tumor microenvironment exerts various effects on cancer progression. Chronic exposure to the inflammatory cytokine interleukin-1 (IL-1) has been shown to impact signaling via the RELA/NF-kB pathway; however, the effects of chronic inflammation on the integration of different inflammatory signaling pathways, such as the interleukin-6 (IL-6)/STAT3 axis, requires further exploration.

methodsWe generated in vitro subline models by exposing the C4-2 and LNCaP PCa cell lines to either IL-1α or IL-1β for several months. We then treated the resulting sublines with acute IL-1 alone, IL-6 alone, or IL-1/IL-6 in combination and assessed for sensitivity to cytokine signaling. We observed changes in proliferation and quantified using Ki-67 immunostaining. Cell proliferation was assessed after siRNA silencing

resultsIL-1/IL-6 signaling in combination enhanced the signaling effects of either cytokine alone, particularly cytostasis. While the chronic IL-1 sublines maintained sensitivity to acute IL-6 signaling, they lost sensitivity to acute IL-1 signaling and did not show the enhanced IL-1/IL-6 cytostatic response. Inhibition of

conclusionsOur work shows that IL-1/RELA and IL-6/STAT3 work in parallel to synergistically induce cytostasis. However, chronic IL-1 exposure selects for cells that attenuate IL-1/RELA signaling, subsequently attenuating IL-1/IL-6 synergy.

Indexed as

cell proliferationcytokineinflammationprostate cancer

Identifiers

PMID41374981
PMCPMC12691196

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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.