Evidence map›Paper›PMID 27197188›Full record

ArticleCancer research2016

Renalase Expression by Melanoma and Tumor-Associated Macrophages Promotes Tumor Growth through a STAT3-Mediated Mechanism.

Lindsay Hollander, Xiaojia Guo, Heino Velazquez, John Chang, Robert Safirstein, Harriet Kluger, Charles Cha, Gary V Desir

Open access · greenAbstract readComparative Study
In one paragraph

Article in Cancer research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

39 citing papers in PubMed, 57 citations in OpenAlex.

  1. Renalase stimulates aldosterone production via PMCA4b/cAMP in NCI-H295R cells.Journal of enzyme inhibition and medicinal chemistry · 2026
    Article
  2. Article
  3. Article
  4. ComprehensiveOncology reports · 2025
    Review
  5. Article
  6. Low Renalase Levels in Newly Diagnosed CML: Dysregulation Sensitive to Modulation by Tyrosine Kinase Inhibitors.Pathophysiology : the official journal of the International Society for Pathophysiology · 2024
    Article
  7. Renalase peptides reduce pancreatitis severity in mice.American journal of physiology. Gastrointestinal and liver physiology · 2024
    Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Renalase: a novel regulator of cardiometabolic and renal diseases.Hypertension research : official journal of the Japanese Society of Hypertension · 2022
    Review
  15. Review
  16. Inhibition of renalase drives tumour rejection by promoting T cell activation.European journal of cancer (Oxford, England : 1990) · 2022
    Article
  17. Article
  18. The Role of Calcium Signaling in Melanoma.International journal of molecular sciences · 2022
    Review
  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

8 authors at 2 institutions in 1 country.

Lindsay HollanderDepartment of Medicine, Yale University, New Haven, Connecticut. Yale School of Medicine, Yale University, New Haven, Connecticut. University of Connecticut, Farmington, Connecticut.
Xiaojia GuoDepartment of Medicine, Yale University, New Haven, Connecticut. Yale School of Medicine, Yale University, New Haven, Connecticut.
Heino VelazquezDepartment of Medicine, Yale University, New Haven, Connecticut. Yale School of Medicine, Yale University, New Haven, Connecticut. VA Connecticut Health Care System, Yale University, New Haven, Connecticut.
John ChangDepartment of Medicine, Yale University, New Haven, Connecticut. VA Connecticut Health Care System, Yale University, New Haven, Connecticut.
Robert SafirsteinDepartment of Medicine, Yale University, New Haven, Connecticut. Yale School of Medicine, Yale University, New Haven, Connecticut. VA Connecticut Health Care System, Yale University, New Haven, Connecticut.
Harriet KlugerDepartment of Medical Oncology, Yale University, New Haven, Connecticut. Yale School of Medicine, Yale University, New Haven, Connecticut.
Charles ChaYale School of Medicine, Yale University, New Haven, Connecticut. VA Connecticut Health Care System, Yale University, New Haven, Connecticut. Department of Surgery, Yale University, New Haven, Connecticut.
Gary V DesirDepartment of Medicine, Yale University, New Haven, Connecticut. Yale School of Medicine, Yale University, New Haven, Connecticut. VA Connecticut Health Care System, Yale University, New Haven, Connecticut. gary.desir@yale.edu.
Yale University · USUniversity of Connecticut · US

Funding

Yale Clinical and Translational Science Award (U Component)UL1TR001863 · NCATS · YALE UNIVERSITY · PI John H. Krystal, LUCILA OHNO-MACHADO · 2016 to 2026
$102.9M
Yale Pathology Tissue Services Shared ResourceP30CA016359 · NCI · YALE UNIVERSITY · PI DAVID L RIMM · 1985 to 2026
$85.0M
Renal Physiology and Phenotyping CoreP30DK079310 · NIDDK · YALE UNIVERSITY · PI ARONSON, PETER S. · 2008 to 2022
$16.8M
The Molecular Physiology of RenalaseR01DK081037 · NIDDK · YALE UNIVERSITY · PI DESIR, GARY V. · 2009 to 2010
$646k
RENALASE DEFICIENCY AND CARDIOVASCULAR COMPLICATIONS OF CHRONIC KIDNEY DISEASERC1DK086402 · NIDDK · YALE UNIVERSITY · PI DESIR, GARY V. · 2010 to 2010
$500k
RENALASE IN ACUTE KIDNEY INJURY: UTILITY AS A BIOMARKER, AND THERAPEUTIC AGENTRC1DK086465 · NIDDK · YALE UNIVERSITY · PI DESIR, GARY V. · 2010 to 2010
$500k
NCATS NIH HHS UL1 TR001863NCI NIH HHS P30 CA016359NIDDK NIH HHS P30 DK079310NIDDK NIH HHS R01 DK081037NIDDK NIH HHS RC1 DK086402NIDDK NIH HHS RC1 DK086465
6 · The paper itself

Abstract

To sustain their proliferation, cancer cells overcome negative-acting signals that restrain their growth and promote senescence and cell death. Renalase (RNLS) is a secreted flavoprotein that functions as a survival factor after ischemic and toxic injury, signaling through the plasma calcium channel PMCA4b to activate the PI3K/AKT and MAPK pathways. We show that RNLS expression is increased markedly in primary melanomas and CD163(+) tumor-associated macrophages (TAM). In clinical specimens, RNLS expression in the tumor correlated inversely with disease-specific survival, suggesting a pathogenic role for RNLS. Attenuation of RNLS by RNAi, blocking antibodies, or an RNLS-derived inhibitory peptide decreased melanoma cell survival, and anti-RNLS therapy blocked tumor growth in vivo in murine xenograft assays. Mechanistic investigations showed that increased apoptosis in tumor cells was temporally related to p38 MAPK-mediated Bax activation and that increased cell growth arrest was associated with elevated expression of the cell-cycle inhibitor p21. Overall, our results established a role for the secreted flavoprotein RNLS in promoting melanoma cell growth and CD163(+) TAM in the tumor microenvironment, with potential therapeutic implications for the management of melanoma. Cancer Res; 76(13); 3884-94. ©2016 AACR.

Indexed as

Gene Expression Regulation, NeoplasticAnimalsApoptosisBiomarkers, TumorBlotting, WesternCase-Control StudiesCell CycleCell ProliferationFemaleFollow-Up StudiesHumansImmunoenzyme TechniquesMacrophagesMaleMelanomaMiceBiomarkers, TumorMonoamine Oxidasep38 Mitogen-Activated Protein KinasesProto-Oncogene Proteins c-aktrenalaseSTAT3 Transcription Factor

Identifiers

PMID27197188
PMCPMC5031238
OpenAlexW2345715545

What OpenQuestion holds

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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.