Evidence map›Paper›PMID 32784606›Full record

ArticleCells2020

Tristetraprolin Posttranscriptionally Downregulates TRAIL Death Receptors.

Won Hyeok Lee, Myung Woul Han, Song Hee Kim, Daseul Seong, Jae Hee An, Hyo Won Chang, Sang Yoon Kim, Seong Who Kim, Jong Cheol Lee

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cells, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.5field-weighted citation impact, top 37% 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

4 citing papers in PubMed, 6 citations in OpenAlex.

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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

9 authors at 1 institution in 1 country.

Won Hyeok LeeDepartment of Otorhinolaryngology, Ulsan University Hospital, University of Ulsan College of Medicine, Ulsan 44033, Korea.
Myung Woul HanDepartment of Otorhinolaryngology, Ulsan University Hospital, University of Ulsan College of Medicine, Ulsan 44033, Korea.
Song Hee KimDepartment of Otorhinolaryngology, Ulsan University Hospital, University of Ulsan College of Medicine, Ulsan 44033, Korea.
Daseul SeongDepartment of Otorhinolaryngology, Ulsan University Hospital, University of Ulsan College of Medicine, Ulsan 44033, Korea.
Jae Hee AnDepartment of Otorhinolaryngology, Ulsan University Hospital, University of Ulsan College of Medicine, Ulsan 44033, Korea.
Hyo Won ChangDepartment of Otolaryngology, Asan Medical Center, University of Ulsan College of Medicine, Seoul 05505, Korea.
Sang Yoon KimDepartment of Otolaryngology, Asan Medical Center, University of Ulsan College of Medicine, Seoul 05505, Korea.
Seong Who KimDepartment of Biochemistry and Molecular Biology, Asan Medical Center, University of Ulsan College of Medicine, Seoul 05505, Korea.
Jong Cheol LeeDepartment of Otorhinolaryngology, GangNeung Asan Hospital, University of Ulsan College of Medicine, Gangneung 25440, Korea.ORCID 0000-0002-2809-5254
Ulsan College · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) has attracted attention as a potential candidate for cancer therapy. However, many primary cancers are resistant to TRAIL, even when combined with standard chemotherapy. The mechanism of TRAIL resistance in cancer cells has not been fully elucidated. The TRAIL death receptor (DR) 3'-untranslated region (3'-UTR) is reported to contain AU-rich elements (AREs) that are important for regulating DR mRNA stability. However, the mechanisms by which DR mRNA stability is determined by its 3'-UTR are unknown. We demonstrate that tristetraprolin (TTP), an ARE-binding protein, has a critical function of regulating DR mRNA stability. DR4 mRNA contains three AREs and DR5 mRNA contains four AREs in 3'-UTR. TTP bound to all three AREs in DR4 and ARE3 in DR5 and enhanced decay of DR4/5 mRNA. TTP overexpression in colon cancer cells changed the TRAIL-sensitive cancer cells to TRAIL-resistant cells, and down-regulation of TTP increased TRAIL sensitivity via DR4/5 expression. Therefore, this study provides a molecular mechanism for enhanced levels of TRAIL DRs in cancer cells and a biological basis for posttranscriptional modification of TRAIL DRs. In addition, TTP status might be a biomarker for predicting TRAIL response when a TRAIL-based treatment is used for cancer.

Indexed as

Cell Line, TumorGene Expression Regulation, NeoplasticHumansNeoplasmsReceptors, TNF-Related Apoptosis-Inducing LigandRNA Processing, Post-TranscriptionalTNF-Related Apoptosis-Inducing LigandTristetraprolinReceptors, TNF-Related Apoptosis-Inducing LigandTNF-Related Apoptosis-Inducing LigandTNFRSF10A protein, humanTNFRSF10B protein, humanTNFSF10 protein, humanTristetraprolinAU-rich elementscancer treatmentdeath receptorposttranscriptional modificationtristetraprolintumor necrosis factor-related apoptosis-inducing ligand

Identifiers

PMID32784606
PMCPMC7465502
OpenAlexW3048167091

What OpenQuestion holds

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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.