Evidence map›Paper›PMID 28855742›Full record

ArticleScientific reports2017

Both p62/SQSTM1-HDAC6-dependent autophagy and the aggresome pathway mediate CDK1 degradation in human breast cancer.

María Galindo-Moreno, Servando Giráldez, Carmen Sáez, Miguel Á Japón, Maria Tortolero, Francisco Romero

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

31 citing papers in PubMed, 45 citations in OpenAlex.

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  14. Extracellular vesicles fromFrontiers in immunology · 2022
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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

6 authors at 2 institutions in 1 country.

María Galindo-MorenoDepartamento de Microbiología, Facultad de Biología, Universidad de Sevilla, Seville, E-41012, Spain.
Servando GiráldezDepartamento de Microbiología, Facultad de Biología, Universidad de Sevilla, Seville, E-41012, Spain.
Carmen SáezInstituto de Biomedicina de Sevilla (IBIS), Hospital Universitario Virgen del Rocío/CSIC/Universidad de Sevilla, Seville, E-41013, Spain.
Miguel Á JapónInstituto de Biomedicina de Sevilla (IBIS), Hospital Universitario Virgen del Rocío/CSIC/Universidad de Sevilla, Seville, E-41013, Spain.
Maria TortoleroDepartamento de Microbiología, Facultad de Biología, Universidad de Sevilla, Seville, E-41012, Spain.
Francisco RomeroDepartamento de Microbiología, Facultad de Biología, Universidad de Sevilla, Seville, E-41012, Spain. frport@us.es.ORCID 0000-0002-9588-6881
Universidad de Sevilla · ESInstituto de Biomedicina de Sevilla · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cyclin-dependent kinase 1 (CDK1) is the central mammalian regulator of cell proliferation and a promising therapeutic target for breast cancer. In fact, CDK1 inhibition downregulates survival and induces apoptosis. Due to its essential role, CDK1 expression and activity are strictly controlled at various levels. We previously described that CDK1 stability is also regulated and that SCF(βTrCP) ubiquitinates CDK1, which is degraded via the lysosomal pathway. In addition, in breast tumors from patients, we found a negative correlation between CDK1 accumulation and βTrCP levels, and a positive correlation with the degree of tumor malignancy. This prompted us to study the molecular mechanism involved in CDK1 clearance. In this report, we determine that both chemotherapeutic agents and proteolytic stress induce CDK1 degradation in human breast cancer MCF7 cells through p62/HDAC6-mediated selective autophagy. On the one hand, CDK1 binds to p62/SQSTM1-LC3 and, on the other hand, it interacts with HDAC6. Both complexes are dependent on the presence of an intact βTrCP-binding motif on CDK1. Furthermore, we also show that CDK1 is recruited to aggresomes in response to proteasome inhibition for an extended period. We propose CDK1 clearance as a potential predictive biomarker of antitumor treatment efficacy.

Indexed as

Gene Expression Regulation, NeoplasticAutophagyCDC2 Protein KinaseHEK293 CellsHeLa CellsHistone Deacetylase 6HumansMCF-7 CellsProteasome Endopeptidase ComplexProtein BindingProtein StabilityProteolysisSequestosome-1 ProteinSignal TransductionSKP Cullin F-Box Protein LigasesUbiquitinationCDC2 Protein KinaseCDK1 protein, humanHDAC6 protein, humanHistone Deacetylase 6Proteasome Endopeptidase ComplexSequestosome-1 ProteinSKP Cullin F-Box Protein LigasesSQSTM1 protein, human

Identifiers

PMID28855742
PMCPMC5577189
OpenAlexW2750517168

What OpenQuestion holds

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LicenceCC BY
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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.