Evidence map›Paper›PMID 28082672›Full record

ArticleThe Journal of biological chemistry2017

NF-κB Signaling Activation Induced by Chloroquine Requires Autophagosome, p62 Protein, and c-Jun N-terminal Kinase (JNK) Signaling and Promotes Tumor Cell Resistance.

Seungwon Yang, Lei Qiang, Ashley Sample, Palak Shah, Yu-Ying He

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
5.7field-weighted citation impact, top 3% 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

38 citing papers in PubMed, 60 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Cells · 2023
    Article
  8. Autophagy Paradox: Strategizing Treatment Modality in Melanoma.Current treatment options in oncology · 2023
    Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
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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

5 authors at 1 institution in 1 country.

Seungwon YangDepartment of Medicine, Section of Dermatology.
Lei QiangDepartment of Medicine, Section of Dermatology.
Ashley SampleDepartment of Medicine, Section of Dermatology; Committee on Cancer Biology, University of Chicago, Chicago, Illinois 60637.
Palak ShahDepartment of Medicine, Section of Dermatology.
Yu-Ying HeDepartment of Medicine, Section of Dermatology; Committee on Cancer Biology, University of Chicago, Chicago, Illinois 60637. Electronic address: yyhe@medicine.bsd.uchicago.edu.
University of Chicago · US

Funding

VIRAL ONCOLOGY CORE FACILITYP30CA014599 · NCI · UNIVERSITY OF CHICAGO · PI MARK W. LINGEN · 1985 to 2026
$122.1M
Re-Engineering Translational Research at the University of ChicagoUL1TR000430 · NCATS · UNIVERSITY OF CHICAGO · PI SOLWAY, JULIAN · 2012 to 2016
$20.2M
Multi-Disciplinary Training Grant in Cancer ResearchT32CA009594 · NCI · UNIVERSITY OF CHICAGO · PI KAY F MACLEOD, Scott A. Oakes · 1989 to 2026
$11.5M
YTHDF2 and UVB damage response in skin cancerR01ES024373 · NIEHS · UNIVERSITY OF CHICAGO · PI HE, YU-YING · 2015 to 2023
$4.3M
Mechanisms of UVA-induced skin cancerR01ES016936 · NIEHS · UNIVERSITY OF CHICAGO · PI HE, YU-YING · 2010 to 2014
$2.2M
NCATS NIH HHS UL1 TR000430NCI NIH HHS P30 CA014599NCI NIH HHS T32 CA009594NIEHS NIH HHS R01 ES016936NIEHS NIH HHS R01 ES024373
6 · The paper itself

Abstract

Macroautophagy (hereafter autophagy) is a catabolic cellular self-eating process by which unwanted organelles or proteins are delivered to lysosomes for degradation through autophagosomes. Although the role of autophagy in cancer has been shown to be context-dependent, the role of autophagy in tumor cell survival has attracted great interest in targeting autophagy for cancer therapy. One family of potential autophagy blockers is the quinoline-derived antimalarial family, including chloroquine (CQ). However, the molecular basis for tumor cell response to CQ remains poorly understood. We show here that in both squamous cell carcinoma cells and melanoma tumor cells, CQ induced NF-κB activation and the expression of its target genes

Indexed as

AnimalsAntimalarialsAntineoplastic AgentsAutophagosomesAutophagyCarcinoma, Squamous CellCell LineCell Line, TumorChloroquineGene Expression Regulation, NeoplasticHumansHypoxia-Inducible Factor 1, alpha SubunitInterleukin-8JNK Mitogen-Activated Protein KinasesMelanomaMiceAntimalarialsAntineoplastic AgentsChloroquineHIF1A protein, humanHypoxia-Inducible Factor 1, alpha SubunitInterleukin-8JNK Mitogen-Activated Protein KinasesNF-kappa BSequestosome-1 ProteinSQSTM1 protein, humanautophagychloroquinemelanomaNF-κBp62 (sequestosome 1(SQSTM1))tumor cell biology

Identifiers

PMID28082672
PMCPMC5336170
OpenAlexW2579027303

What OpenQuestion holds

Textmetadata
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.