Evidence map›Paper›PMID 28857256›Full record

ArticleJournal of cellular biochemistry2018

Autophagy-dependent crosstalk between GILT and PAX-3 influences radiation sensitivity of human melanoma cells.

Jessica D Hathaway-Schrader, Bently P Doonan, Azim Hossain, Faisal F Y Radwan, Lixia Zhang, Azizul Haque

Abstract read
In one paragraph

Article in Journal of cellular biochemistry, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.0field-weighted citation impact, top 22% 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

15 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. 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 1 institution in 1 country.

Jessica D Hathaway-SchraderDepartment of Microbiology and Immunology, Hollings Cancer Center, and Children's Research Institute, Medical University of South Carolina, Charleston, South Carolina.
Bently P DoonanDepartment of Microbiology and Immunology, Hollings Cancer Center, and Children's Research Institute, Medical University of South Carolina, Charleston, South Carolina.
Azim HossainDepartment of Microbiology and Immunology, Hollings Cancer Center, and Children's Research Institute, Medical University of South Carolina, Charleston, South Carolina.
Faisal F Y RadwanDepartment of Microbiology and Immunology, Hollings Cancer Center, and Children's Research Institute, Medical University of South Carolina, Charleston, South Carolina.
Lixia ZhangDepartment of Microbiology and Immunology, Hollings Cancer Center, and Children's Research Institute, Medical University of South Carolina, Charleston, South Carolina.
Azizul HaqueDepartment of Microbiology and Immunology, Hollings Cancer Center, and Children's Research Institute, Medical University of South Carolina, Charleston, South Carolina.ORCID 0000-0002-6386-9390
Medical University of South Carolina · US

Funding

Translational Science Laboratory Shared ResourceP30CA138313 · NCI · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI RAYMOND N. DUBOIS · 2009 to 2026
$42.7M
Disruption of HLA Class II-Mediated Immune Recognition of B-Cell LymphomasR01CA129560 · NCI · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI HAQUE, AZIZUL · 2009 to 2013
$1.5M
NCI NIH HHS P30 CA138313NCI NIH HHS R01 CA129560
6 · The paper itself

Abstract

Melanoma represents an ever-increasing problem in the western world as incidence rates continue to climb. Though manageable during early stages, late stage metastatic disease is highly resistant to current intervention. We have previously shown that gamma-interferon-inducible lysosomal thiol-reductase (GILT) enhances HLA class II antigen processing and immune detection of human melanoma cells. Here we report that GILT expression inhibits a potential target, paired box-3 (PAX-3) protein, in late stage human metastatic melanoma. We also show that GILT transfection or induction by IFN-γ, decreases PAX-3 protein expression while upregulating the expression of Daxx, which is also a repressor of PAX-3. Confocal microscopic analysis demonstrated that GILT co-localizes with PAX-3 protein, but not with Daxx within melanoma cells. Immunoprecipitation and immunoblotting studies suggest that GILT expression negatively regulates PAX-3 through the autophagy pathway, potentially resulting in increased susceptibility to conventional treatment in the form of chemotherapy or radiotherapy. While high-dose radiation is a common treatment for melanoma patients, our data suggest that GILT expression significantly increased the susceptibility of melanoma cells to low-dose radiation therapy via upregulation of tumor suppressor protein p53. Overall, these data suggest that GILT has multiple roles in inducing human melanoma cells as better targets for radiation and immunotherapy.

Indexed as

Adaptor Proteins, Signal TransducingAutophagyCell Line, TumorCo-Repressor ProteinsGene Expression Regulation, NeoplasticHumansLysosomesMelanomaMolecular ChaperonesNeoplasm StagingNuclear ProteinsOxidoreductases Acting on Sulfur Group DonorsPAX3 Transcription FactorSignal TransductionTumor Suppressor Protein p53Adaptor Proteins, Signal TransducingCo-Repressor ProteinsDAXX protein, humanIFI30 protein, humanMolecular ChaperonesNuclear ProteinsOxidoreductases Acting on Sulfur Group DonorsPAX3 protein, humanPAX3 Transcription FactorTP53 protein, humanTumor Suppressor Protein p53autophagyDAXXGILTmelanomaPAX-3radiation

Identifiers

PMID28857256
PMCPMC5747991
OpenAlexW2752897707

What OpenQuestion holds

Textmetadata
LicenceTDM
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.