Evidence map›Paper›PMID 26871465›Full record

ArticleOncotarget2016

HIF-3α1 promotes colorectal tumor cell growth by activation of JAK-STAT3 signaling.

Xiang Xue, Kylie Jungles, Gunseli Onder, Jalal Samhoun, Balázs Győrffy, Karin M Hardiman

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
0.9field-weighted citation impact, top 27% 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

21 citing papers in PubMed, 32 citations in OpenAlex.

  1. Review
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  6. The emerging role of hypoxia and environmental factors in inflammatory bowel disease.Toxicological sciences : an official journal of the Society of Toxicology · 2024
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. The Hypoxia-Long Noncoding RNA Interaction in Solid Cancers.International journal of molecular sciences · 2021
    Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. TheFrontiers in endocrinology · 2020
    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

6 authors at 3 institutions in 2 countries.

Xiang XueDepartment of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, MI, USA.
Kylie JunglesDepartment of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, MI, USA.
Gunseli OnderDepartment of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, MI, USA.
Jalal SamhounDepartment of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, MI, USA.
Balázs GyőrffyMTA TTK Lendület Cancer Biomarker Research Group, MTA-SE Pediatrics and Nephrology Research Group, Semmelweis University 2nd Department of Pediatrics, Budapest, Hungary.
Karin M HardimanDepartment of Surgery, University of Michigan, Ann Arbor, MI, USA.
University of Michigan–Ann Arbor · USSaint Mary's College · USSemmelweis University · HU

Funding

Interfacing computation and engineering with digestive and metabolic physiologyR25DK088752 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI MACDOUGALD, ORMOND A · 2010 to 2020
$1.1M
NIDDK NIH HHS R25 DK088752
6 · The paper itself

Abstract

Hypoxic environment is critical in colorectal cancer (CRC) development. Most studies have mainly focused on hypoxia-inducible factor (HIF)-1α and HIF-2α as the major hypoxic transcription factors in CRC development and progression. However, the role of HIF-3α in CRC is not clear. Here we found that HIF-3α protein was increased in colorectal tumors from both mouse models and human patients. Moreover, increased HIF-3α expression was correlated with decreased survival. Overexpression of a long isoform of HIF-3α, HIF-3α1, increased cell growth in two CRC cell lines. Surprisingly, overexpressed HIF-3α1 was localized to the cytosol and increased phosphorylated signal transducer and activator of transcription 3 (p-STAT3). STAT3 inhibition effectively reduced p-STAT3 levels and cell growth induced by HIF-3α1. The activation of p-STAT3 was independent of the transcriptional activity of HIF-3α1. However, the inhibition of the upstream regulator Janus kinase (JAK) abolished HIF-3α1-induced p-STAT3 and cell growth. Together, these results demonstrated that HIF-3α1 promotes CRC cell growth by activation of the JAK-STAT3 signaling pathway through non-canonical transcription-independent mechanisms.

Indexed as

AnimalsApoptosis Regulatory ProteinsBasic Helix-Loop-Helix ProteinsCell HypoxiaCell Line, TumorCell ProliferationColorectal NeoplasmsHT29 CellsHumansJanus KinasesMiceRepressor ProteinsSignal TransductionSTAT3 Transcription FactorTranscription FactorsApoptosis Regulatory ProteinsBasic Helix-Loop-Helix ProteinsHIF3A protein, humanHif3a protein, mouseJanus KinasesRepressor ProteinsSTAT3 protein, humanStat3 protein, mouseSTAT3 Transcription FactorTranscription Factorsactivator of transcription 3colorectal cancerhypoxia-inducible factor-3αJanus kinasesignal transducer

Identifiers

PMID26871465
PMCPMC4905494
OpenAlexW2284707517

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.