Evidence map›Paper›PMID 35853811›Full record

ArticleEBioMedicine2022

The ubiquitin-ligase TRAF6 and TGFβ type I receptor form a complex with Aurora kinase B contributing to mitotic progression and cytokinesis in cancer cells.

Jie Song, Yang Zhou, Ihor Yakymovych, Alexej Schmidt, Chunyan Li, Carl-Henrik Heldin, Maréne Landström

Open access · goldAbstract read
In one paragraph

Article in EBioMedicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

10 citing papers in PubMed, 21 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

7 authors at 2 institutions in 1 country.

Jie SongDepartment of Medical Biosciences, Pathology, Umeå University, SE-901 85 Umeå, Sweden.
Yang ZhouDepartment of Medical Biosciences, Pathology, Umeå University, SE-901 85 Umeå, Sweden.
Ihor YakymovychDepartment of Medical Biochemistry and Microbiology, Science for Life Laboratory, Uppsala University, Box 582, SE-751 23 Uppsala, Sweden.
Alexej SchmidtDepartment of Medical Biosciences, Pathology, Umeå University, SE-901 85 Umeå, Sweden.
Chunyan LiDepartment of Medical Biosciences, Pathology, Umeå University, SE-901 85 Umeå, Sweden.
Carl-Henrik HeldinDepartment of Medical Biochemistry and Microbiology, Science for Life Laboratory, Uppsala University, Box 582, SE-751 23 Uppsala, Sweden.
Maréne LandströmDepartment of Medical Biosciences, Pathology, Umeå University, SE-901 85 Umeå, Sweden. Electronic address: marene.landstrom@umu.se.
Umeå University · SEUppsala University · SE

Funding

European Research Council 787472
6 · The paper itself

Abstract

backgroundTransforming growth factor β (TGFβ) is overexpressed in several advanced cancer types and promotes tumor progression. We have reported that the intracellular domain (ICD) of TGFβ receptor (TβR) I is cleaved by proteolytic enzymes in cancer cells, and then translocated to the nucleus in a manner dependent on the endosomal adaptor proteins APPL1/2, driving an invasiveness program. How cancer cells evade TGFβ-induced growth inhibition is unclear.

methodsWe performed microarray analysis to search for genes regulated by APPL1/2 proteins in castration-resistant prostate cancer (CRPC) cells. We investigated the role of TβRI and TRAF6 in mitosis in cancer cell lines cultured in 10% FBS in the absence of exogenous TGFβ. The molecular mechanism of the ubiquitination of AURKB by TRAF6 in mitosis and the formation of AURKB-TβRI complex in cancer cell lines and tissue microarrays was also studied.

findingsDuring mitosis and cytokinesis, AURKB-TβRI complexes formed in midbodies in CRPC and KELLY neuroblastoma cells. TRAF6 induced polyubiquitination of AURKB on K85 and K87, protruding on the surface of AURKB to facilitate its activation. AURKB-TβRI complexes in patient's tumor tissue sections correlated with the malignancy of prostate cancer.

interpretationThe AURKB-TβRI complex may become a prognostic biomarker for patients with risk of developing aggressive PC.

fundingSwedish Medical Research Council (2019-01598, ML; 2015-02757 and 2020-01291, CHH), the Swedish Cancer Society (20 0964, ML), a regional agreement between Umeå University and Region Västerbotten (ALF; RV-939377, -967041, -970057, ML). The European Research Council (787472, CHH). KAW 2019.0345, and the Kempe Foundation SMK-1866; ML. National Microscopy Infrastructure (NMI VR-RFI 2016-00968).

Indexed as

Prostatic Neoplasms, Castration-ResistantTNF Receptor-Associated Factor 6Aurora Kinase BCell Line, TumorCytokinesisHumansIntracellular Signaling Peptides and ProteinsLigasesMaleReceptor, Transforming Growth Factor-beta Type ITransforming Growth Factor betaUbiquitinAURKB protein, humanAurora Kinase BIntracellular Signaling Peptides and ProteinsLigasesReceptor, Transforming Growth Factor-beta Type ITGFBR1 protein, humanTifab protein, humanTNF Receptor-Associated Factor 6Transforming Growth Factor betaUbiquitinAPPL1AURKBCancerMitosisTRAF6TβRI

Identifiers

PMID35853811
PMCPMC9386726
OpenAlexW4285600273

What OpenQuestion holds

Textmetadata
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.