Evidence map›Paper›PMID 25851605›Full record

ArticleMolecular biology of the cell2015

Cyclin-dependent kinase 5 acts as a critical determinant of AKT-dependent proliferation and regulates differential gene expression by the androgen receptor in prostate cancer cells.

Julia Lindqvist, Susumu Y Imanishi, Elin Torvaldson, Marjo Malinen, Mika Remes, Fanny Örn, Jorma J Palvimo, John E Eriksson

Open access · greenAbstract read
In one paragraph

Article in Molecular biology of the cell, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
4.3field-weighted citation impact, top 5% 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

27 citing papers in PubMed, 42 citations in OpenAlex.

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  8. Cdk5 regulates IP3R1-mediated CaCellular and molecular life sciences : CMLS · 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

8 authors at 2 institutions in 1 country.

Julia LindqvistDepartment of Biosciences, Faculty of Science and Engineering, Åbo Akademi University, FI-20520 Turku, Finland Turku Centre for Biotechnology, University of Turku and Åbo Akademi University, FI-20520 Turku, Finland.
Susumu Y ImanishiTurku Centre for Biotechnology, University of Turku and Åbo Akademi University, FI-20520 Turku, Finland.
Elin TorvaldsonDepartment of Biosciences, Faculty of Science and Engineering, Åbo Akademi University, FI-20520 Turku, Finland Turku Centre for Biotechnology, University of Turku and Åbo Akademi University, FI-20520 Turku, Finland.
Marjo MalinenInstitute of Biomedicine/Medical Biochemistry, University of Eastern Finland, and Department of Pathology, Kuopio University Hospital, FI-70211 Kuopio, Finland.
Mika RemesDepartment of Biosciences, Faculty of Science and Engineering, Åbo Akademi University, FI-20520 Turku, Finland.
Fanny ÖrnDepartment of Biosciences, Faculty of Science and Engineering, Åbo Akademi University, FI-20520 Turku, Finland Turku Centre for Biotechnology, University of Turku and Åbo Akademi University, FI-20520 Turku, Finland.
Jorma J PalvimoInstitute of Biomedicine/Medical Biochemistry, University of Eastern Finland, and Department of Pathology, Kuopio University Hospital, FI-70211 Kuopio, Finland.
John E ErikssonDepartment of Biosciences, Faculty of Science and Engineering, Åbo Akademi University, FI-20520 Turku, Finland Turku Centre for Biotechnology, University of Turku and Åbo Akademi University, FI-20520 Turku, Finland john.eriksson@abo.fi.
Åbo Akademi University · FIUniversity of Eastern Finland · FI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Contrary to cell cycle-associated cyclin-dependent kinases, CDK5 is best known for its regulation of signaling processes in differentiated cells and its destructive activation in Alzheimer's disease. Recently, CDK5 has been implicated in a number of different cancers, but how it is able to stimulate cancer-related signaling pathways remains enigmatic. Our goal was to study the cancer-promoting mechanisms of CDK5 in prostate cancer. We observed that CDK5 is necessary for proliferation of several prostate cancer cell lines. Correspondingly, there was considerable growth promotion when CDK5 was overexpressed. When examining the reasons for the altered proliferation effects, we observed that CDK5 phosphorylates S308 on the androgen receptor (AR), resulting in its stabilization and differential expression of AR target genes including several growth-priming transcription factors. However, the amplified cell growth was found to be separated from AR signaling, further corroborated by CDK5-dependent proliferation of AR null cells. Instead, we found that the key growth-promoting effect was due to specific CDK5-mediated AKT activation. Down-regulation of CDK5 repressed AKT phosphorylation by altering its intracellular localization, immediately followed by prominent cell cycle inhibition. Taken together, these results suggest that CDK5 acts as a crucial signaling hub in prostate cancer cells by controlling androgen responses through AR, maintaining and accelerating cell proliferation through AKT activation, and releasing cell cycle breaks.

Indexed as

Cell ProliferationGene Expression Regulation, NeoplasticCyclin-Dependent Kinase 5HumansMalePhosphorylationProstatic NeoplasmsProto-Oncogene Proteins c-aktReceptors, AndrogenSignal TransductionAR protein, humanCDK5 protein, humanCyclin-Dependent Kinase 5Proto-Oncogene Proteins c-aktReceptors, Androgen

Identifiers

PMID25851605
PMCPMC4472009
OpenAlexW2162704197

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.