Evidence map›Paper›PMID 27491285›Full record

ArticleBMC cancer2016

S6Ks isoforms contribute to viability, migration, docetaxel resistance and tumor formation of prostate cancer cells.

Camila L Amaral, Lidia B Freitas, Rodrigo E Tamura, Mariana R Tavares, Isadora C B Pavan, Marcio C Bajgelman, Fernando M Simabuco

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 10% 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

32 citing papers in PubMed, 1 synthesis or guideline pooled it, 54 citations in OpenAlex.

  1. Pooled it
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  17. Ribosomal Protein S6: A Potential Therapeutic Target against Cancer?International journal of molecular sciences · 2021
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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 3 institutions in 1 country.

Camila L AmaralLaboratory of Disorders of Metabolism, School of Applied Sciences, University of Campinas, R. Pedro Zaccaria, 1300, sala LA 421, 13484-350, Limeira, São Paulo, Brazil.
Lidia B FreitasLaboratory of Disorders of Metabolism, School of Applied Sciences, University of Campinas, R. Pedro Zaccaria, 1300, sala LA 421, 13484-350, Limeira, São Paulo, Brazil.
Rodrigo E TamuraViral Vector Laboratory, Center for Translational Investigation in Oncology/LIM24, Cancer Institute of São Paulo, School of Medicine, University of São Paulo, São Paulo, Brazil.
Mariana R TavaresLaboratory of Disorders of Metabolism, School of Applied Sciences, University of Campinas, R. Pedro Zaccaria, 1300, sala LA 421, 13484-350, Limeira, São Paulo, Brazil.
Isadora C B PavanLaboratory of Disorders of Metabolism, School of Applied Sciences, University of Campinas, R. Pedro Zaccaria, 1300, sala LA 421, 13484-350, Limeira, São Paulo, Brazil.
Marcio C BajgelmanBrazilian Biosciences National Laboratory, Brazilian National Center for Research in Energy and Materials, Campinas, São Paulo, Brazil.
Fernando M SimabucoLaboratory of Disorders of Metabolism, School of Applied Sciences, University of Campinas, R. Pedro Zaccaria, 1300, sala LA 421, 13484-350, Limeira, São Paulo, Brazil. simabuco@gmail.com.
Universidade Estadual de Campinas (UNICAMP) · BRBrazilian Biosciences National Laboratory · BRUniversidade de São Paulo · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe S6 Kinase (S6K) proteins are some of the main downstream effectors of the mammalian Target Of Rapamycin (mTOR) and act as key regulators of protein synthesis and cell growth. S6K is overexpressed in a variety of human tumors and is correlated to poor prognosis in prostate cancer. Due to the current urgency to identify factors involved in prostate cancer progression, we aimed to reveal the cellular functions of three S6K isoforms-p70-S6K1, p85-S6K1 and p54-S6K2-in prostate cancer, as well as their potential as therapeutic targets.

methodsIn this study we performed S6K knockdown and overexpression and investigated its role in prostate cancer cell proliferation, colony formation, viability, migration and resistance to docetaxel treatment. In addition, we measured tumor growth in Nude mice injected with PC3 cells overexpressing S6K isoforms and tested the efficacy of a new available S6K1 inhibitor in vitro.

resultsS6Ks overexpression enhanced PC3-luc cell line viability, migration, resistance to docetaxel and tumor formation in Nude mice. Only S6K2 knockdown rendered prostate cancer cells more sensitive to docetaxel. S6K1 inhibitor PF-4708671 was particularly effective for reducing migration and proliferation of PC3 cell line.

conclusionsThese findings demonstrate that S6Ks play an important role in prostate cancer progression, enhancing cell viability, migration and chemotherapy resistance, and place both S6K1 and S6K2 as a potential targets in advanced prostate cancer. We also provide evidence that S6K1 inhibitor PF-4708671 may be considered as a potential drug for prostate cancer treatment.

Indexed as

AnimalsAntineoplastic AgentsBlotting, WesternCell Line, TumorCell MovementCell SurvivalDocetaxelDrug Resistance, NeoplasmEnzyme InhibitorsGene Knockdown TechniquesHeterograftsHumansIsoenzymesMaleMiceMice, NudeAntineoplastic AgentsDocetaxelEnzyme InhibitorsIsoenzymesRibosomal Protein S6 KinasesTaxoidsCancermTORS6K

Identifiers

PMID27491285
PMCPMC4974797
OpenAlexW2483437652

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.