Evidence map›Paper›PMID 29843216›Full record

ArticleCancer biomarkers : section A of Disease markers2018

Transcription factor KLF13 inhibits AKT activation and suppresses the growth of prostate carcinoma cells.

Qiang Wang, Ruixian Peng, Boshi Wang, Jifeng Wang, Wandong Yu, Yongzhong Liu, Guowei Shi

Open access · hybridAbstract read
In one paragraph

Article in Cancer biomarkers : section A of Disease markers, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

25 citing papers in PubMed, 38 citations in OpenAlex.

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  6. Genome-Wide Identification, Evolution, and miRNA-22 Regulation ofAnimals : an open access journal from MDPI · 2024
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  10. Molecular Mechanisms of IL18 in Disease.International journal of molecular sciences · 2023
    Review
  11. Review
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  13. Article
  14. Article
  15. SP and KLF Transcription Factors in Cancer Metabolism.International journal of molecular sciences · 2022
    Review
  16. Article
  17. Article
  18. Article
  19. Article
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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.

Qiang WangDepartment of Urology, The Fifth People's Hospital of Shanghai, Fudan University, Shanghai, China.
Ruixian PengDepartment of Urology, The Fifth People's Hospital of Shanghai, Fudan University, Shanghai, China.
Boshi WangState Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, Renji Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China.
Jifeng WangDepartment of Urology, The Fifth People's Hospital of Shanghai, Fudan University, Shanghai, China.
Wandong YuDepartment of Urology, The Fifth People's Hospital of Shanghai, Fudan University, Shanghai, China.
Yongzhong LiuState Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, Renji Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China.
Guowei ShiDepartment of Urology, The Fifth People's Hospital of Shanghai, Fudan University, Shanghai, China.
Fudan University · CNRenji Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundKrüppel-like factor 13 (KLF13), a member of the KLF family, is involved in the development of immunological diseases and tumor progression. However, the expression patterns and potential functions of KLF13 in prostate carcinoma are still unknown. Here, we aimed to study the roles and mechanisms of KLF13 in prostate cancer.

methodsThe expression levels of KLF13 was detected by Immunohistochemistry in prostate tumor tissues and the paired non-tumor tissues. The effects of KLF13 up-regulation was tested by performing CCK8, cell colon formation, flow cytometric analysis and measurement of tumor proliferation in nude mice. Signaling pathway was analyzed by Western blot.

resultsThe current study, for the first time, found that KLF13 was downregulated in prostate tumor tissues as compared to the paired non-tumor tissues. The overexpression of KLF13 dramatically inhibited cell proliferation and induced apoptosis by suppressing the AKT pathway in human prostate cancer cells. Moreover, the ectopic expression of KLF13 efficiently delayed the onset of PC3 xenografts and inhibited the tumor growth in vivo.

conclusionsKLF13 functions as a tumor suppressor protein in PCa, and the pharmacological activation of KLF13 might represent a potential approach for the treatment of prostate cancer.

Indexed as

AnimalsApoptosisBiomarkers, TumorCell Cycle ProteinsCell Line, TumorCell ProliferationCell SurvivalDisease Models, AnimalEnzyme ActivationGene ExpressionGene Expression Regulation, NeoplasticHeterograftsHumansImmunohistochemistryKruppel-Like Transcription FactorsMaleBiomarkers, TumorCell Cycle ProteinsKLF13 protein, humanKruppel-Like Transcription FactorsProto-Oncogene Proteins c-aktRepressor ProteinsAKT pathwayapoptosisImmunohistochemistryKrüppel-like factor 13prostate cancer

Identifiers

PMID29843216
PMCPMC6218114
OpenAlexW2803379925

What OpenQuestion holds

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LicenceCC BY-NC
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Registered trials

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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.