Evidence map›Paper›PMID 24153058›Full record

ArticleCancer biology & therapy2013

The DeISGylase USP18 limits TRAIL-induced apoptosis through the regulation of TRAIL levels: Cellular levels of TRAIL influences responsiveness to TRAIL-induced apoptosis.

Ivana Manini, Andrea Sgorbissa, Harish Potu, Andrea Tomasella, Claudio Brancolini

Open access · bronzeAbstract read
In one paragraph

Article in Cancer biology & therapy, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.6field-weighted citation impact, top 31% 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

11 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Deubiquitinases: Modulators of Different Types of Regulated Cell Death.International journal of molecular sciences · 2021
    Review
  3. Emerging Roles of USP18: From Biology to Pathophysiology.International journal of molecular sciences · 2020
    Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Multiple functions of USP18.Cell death & disease · 2016
    Review
  11. 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

5 authors at 1 institution in 1 country.

Ivana ManiniDipartimento di Scienze Mediche e Biologiche and MATI Center of Excellence; Università degli Studi di Udine; Udine, Italy.
Andrea SgorbissaDipartimento di Scienze Mediche e Biologiche and MATI Center of Excellence; Università degli Studi di Udine; Udine, Italy.
Harish PotuDipartimento di Scienze Mediche e Biologiche and MATI Center of Excellence; Università degli Studi di Udine; Udine, Italy.
Andrea TomasellaDipartimento di Scienze Mediche e Biologiche and MATI Center of Excellence; Università degli Studi di Udine; Udine, Italy.
Claudio BrancoliniDipartimento di Scienze Mediche e Biologiche and MATI Center of Excellence; Università degli Studi di Udine; Udine, Italy.
University of Udine · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) is a promising molecule for anti-cancer therapies. Unfortunately, cancer cells frequently acquire resistance to rhTRAIL. Various co-treatments have been proposed to overcome apoptosis resistance to TRAIL. Here we show that downregulation of the deISGylase USP18 sensitizes cancer cells to rhTRAIL, whereas, elevate levels of USP18 inhibit TRAIL-induced apoptosis, in a deISGylase-independent manner. USP18 influences TRAIL signaling through the control of the IFN autocrine loop. In fact, cells with downregulated USP18 expression augment the expression of cellular TRAIL. Downregulation of cellular TRAIL abrogates the synergism between TRAIL and USP18 siRNA and also limits cell death induced by rhTRAIL. By comparing the apoptotic responsiveness to TRAIL in a panel of cancer cell lines, we have discovered a correlation between TRAIL levels and the apoptotic susceptibility to rhTRAIL, In cells expressing high levels of TRAIL-R2 susceptibility to rhTRAIL correlates with TRAIL expression. In conclusion, we propose that cellular TRAIL is an additional factor that can influence the apoptotic response to rhTRAIL.

Indexed as

ApoptosisCell Line, TumorDrug Resistance, NeoplasmEndopeptidasesHumansInterferonsRecombinant ProteinsTNF-Related Apoptosis-Inducing LigandUbiquitin ThiolesteraseEndopeptidasesInterferonsRecombinant ProteinsTNF-Related Apoptosis-Inducing LigandUbiquitin ThiolesteraseUSP18 protein, humanautocrine loopIFNARIFN-αTRAILTRAIL-R2USP18

Identifiers

PMID24153058
PMCPMC3912039
OpenAlexW2075425309

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.