Evidence map›Paper›PMID 33953348›Full record

ReviewCell death and differentiation2021

MLKL in cancer: more than a necroptosis regulator.

Sofie Martens, Jolien Bridelance, Ria Roelandt, Peter Vandenabeele, Nozomi Takahashi

Open access · bronzeAbstract readReview
In one paragraph

Review in Cell death and differentiation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 111 papers.

0numbers the graph read from it
0cells of the map it votes in
111citing papers in PubMed
10.6field-weighted citation impact, top 1% 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

111 citing papers in PubMed, 167 citations in OpenAlex.

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51 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

5 authors at 2 institutions in 1 country.

Sofie MartensCell Death and Inflammation Lab, VIB Center for Inflammation Research, Ghent, Belgium.
Jolien BridelanceCell Death and Inflammation Lab, VIB Center for Inflammation Research, Ghent, Belgium.
Ria RoelandtCell Death and Inflammation Lab, VIB Center for Inflammation Research, Ghent, Belgium.
Peter Vandenabeele *Cell Death and Inflammation Lab, VIB Center for Inflammation Research, Ghent, Belgium. Peter.Vandenabeele@irc.vib-ugent.be.ORCID http://orcid.org/0000-0002-6669-8822
Nozomi Takahashi *Cell Death and Inflammation Lab, VIB Center for Inflammation Research, Ghent, Belgium.
Ghent University · BEVIB-UGent Center for Inflammation Research · BE

Funding

Belgian National Fund for Scientific Research | Fonds pour la Formation à la Recherche dans l'Industrie et dans l'Agriculture (Training Fund for Research in Industry and Agriculture) EOS MODEL-IDI Grant 30826052,esearch grants G.0E04.16N, G.0C76.18N, G.0B71.18N, G.0B96.20NBijzonder Onderzoeksfonds (Special Research Fund) Methusalem BOF16/MET_V/007, iBOF20/IBF/039 ATLANTISStichting Tegen Kanker (Belgian Foundation Against Cancer) FAF-F/2016/865, F/2020/1505
6 · The paper itself

Abstract

Mixed lineage kinase domain-like protein (MLKL) emerged as executioner of necroptosis, a RIPK3-dependent form of regulated necrosis. Cell death evasion is one of the hallmarks of cancer. Besides apoptosis, some cancers suppress necroptosis-associated mechanisms by for example epigenetic silencing of RIPK3 expression. Conversely, necroptosis-elicited inflammation by cancer cells can fuel tumor growth. Recently, necroptosis-independent functions of MLKL were unraveled in receptor internalization, ligand-receptor degradation, endosomal trafficking, extracellular vesicle formation, autophagy, nuclear functions, axon repair, neutrophil extracellular trap (NET) formation, and inflammasome regulation. Little is known about the precise role of MLKL in cancer and whether some of these functions are involved in cancer development and metastasis. Here, we discuss current knowledge and controversies on MLKL, its structure, necroptosis-independent functions, expression, mutations, and its potential role as a pro- or anti-cancerous factor. Analysis of MLKL expression patterns reveals that MLKL is upregulated by type I/II interferon, conditions of inflammation, and tissue injury. Overall, MLKL may affect cancer development and metastasis through necroptosis-dependent and -independent functions.

Indexed as

AnimalsDisease Models, AnimalHumansMiceNecroptosisNeoplasmsProtein KinasesMLKL protein, mouseProtein Kinases

Identifiers

PMID33953348
PMCPMC8184805
OpenAlexW3158840936

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.