Evidence map›Paper›PMID 31462408›Full record

ArticleCancer immunology research2019

STING Signaling in Melanoma Cells Shapes Antigenicity and Can Promote Antitumor T-cell Activity.

Rana Falahat, Patricio Perez-Villarroel, Adam W Mailloux, Genyuan Zhu, Shari Pilon-Thomas, Glen N Barber, James J Mulé

Abstract read
In one paragraph

Article in Cancer immunology research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.

0numbers the graph read from it
0cells of the map it votes in
69citing 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

69 citing papers in PubMed.

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  10. Structural immunotherapy: Harnessing chemical design to build powerful next-generation therapeutics.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  11. Chemokine/cytokine-releasing biomaterials induce in situ tertiary lymphoid-like structures and enhance antitumor immunity.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  12. cGAS-STING signaling in melanoma: regulation and therapeutic targeting.Naunyn-Schmiedeberg's archives of pharmacology · 2025
    Review
  13. Review
  14. Article
  15. A versatile immunomodulated nanoCRISPR converter augments the susceptibility and visibility of tumors to the immune system.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
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9 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

7 authors.

Rana FalahatImmunology Program, Moffitt Cancer Center, Tampa, Florida.
Patricio Perez-VillarroelImmunology Program, Moffitt Cancer Center, Tampa, Florida.
Adam W MaillouxImmunology Program, Moffitt Cancer Center, Tampa, Florida.
Genyuan ZhuImmunology Program, Moffitt Cancer Center, Tampa, Florida.
Shari Pilon-ThomasImmunology Program, Moffitt Cancer Center, Tampa, Florida.
Glen N BarberDepartment of Cell Biology, University of Miami Miller School of Medicine, Miami, Florida.
James J MuléImmunology Program, Moffitt Cancer Center, Tampa, Florida. James.Mule@moffitt.org.ORCID 0000-0001-7354-0516

Funding

TRANSLATIONAL RESEARCHP30CA076292 · NCI · UNIVERSITY OF SOUTH FLORIDA · PI KENNETH Lynn WRIGHT · 1998 to 2026
$93.5M
Tissue, Pathology and BioinformaticsP50CA168536 · NCI · H. LEE MOFFITT CANCER CTR & RES INST · PI MULE, JAMES J. · 2013 to 2017
$8.5M
Biomarkers and Resistance Mechanisms in Melanoma T-cell TherapyR01CA184845 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI HWU, PATRICK, MULE, JAMES J. · 2014 to 2018
$1.7M
Designing Lymph Nodes for Cancer ImmunotherapyR01CA148995 · NCI · H. LEE MOFFITT CANCER CTR & RES INST · PI MULE, JAMES J. · 2010 to 2014
$1.7M
NCI NIH HHS P30 CA076292NCI NIH HHS P50 CA168536NCI NIH HHS R01 CA148995NCI NIH HHS R01 CA184845
6 · The paper itself

Abstract

STING (stimulator of IFN genes) signaling is an innate immune pathway for induction of a spontaneous antitumor T-cell response against certain immunogenic tumors. Although antigen-presenting cells are known to be involved in this process, insight into the participation of tumor cell-intrinsic STING signaling remains weak. In this study, we find diversity in the regulation of STING signaling across a panel of human melanoma cell lines. We show that intact activation of STING signaling in a subset of human melanoma cell lines enhances both their antigenicity and susceptibility to lysis by human melanoma tumor-infiltrating lymphocytes (TIL) through the augmentation of MHC class I expression. Conversely, defects in the STING signaling pathway protect melanoma cells from increased immune recognition by TILs and limit their sensitivity to TIL lysis. Based on these findings, we propose that defects in tumor cell-intrinsic STING signaling can mediate not only tumor immune evasion but also resistance to TIL-based immunotherapies.

Indexed as

Cyclic Guanosine Monophosphate-Adenosine Monophosphate SynthaseCytotoxicity, ImmunologicHistocompatibility Antigens Class IHumansLymphocytes, Tumor-InfiltratingMelanomaMembrane ProteinsNucleotidyltransferasesSignal TransductionSTING ProteinTumor Cells, CulturedTumor EscapeUp-RegulationcGAS protein, humanCyclic Guanosine Monophosphate-Adenosine Monophosphate SynthaseHistocompatibility Antigens Class IMembrane ProteinsNucleotidyltransferasesSTING1 protein, humanSTING Protein

Identifiers

PMID31462408
PMCPMC6825582

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Registered trials

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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.