Evidence map›Paper›PMID 24585183›Full record

ArticleInternational journal of oncology2014

Downregulation of the tumor suppressor HSPB7, involved in the p53 pathway, in renal cell carcinoma by hypermethylation.

Jiaying Lin, Zhenzhong Deng, Chizu Tanikawa, Taro Shuin, Tsuneharu Miki, Koichi Matsuda, Yusuke Nakamura

Open access · hybridAbstract read
In one paragraph

Article in International journal of oncology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.3field-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

20 citing papers in PubMed, 40 citations in OpenAlex.

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  11. Genomic and epigenetic aberrations of chromosome 1p36.13 have prognostic implications in malignancies.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2020
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  19. Molecular genetic response to varied wavelengths of light in Xiphophorus maculatus skin.Comparative biochemistry and physiology. Toxicology & pharmacology : CBP · 2015
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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.

Jiaying LinLaboratory of Molecular Medicine, Human Genome Center, Institute of Medical Science, University of Tokyo, Tokyo 108-8639, Japan.
Zhenzhong DengLaboratory of Molecular Medicine, Human Genome Center, Institute of Medical Science, University of Tokyo, Tokyo 108-8639, Japan.
Chizu TanikawaLaboratory of Molecular Medicine, Human Genome Center, Institute of Medical Science, University of Tokyo, Tokyo 108-8639, Japan.
Taro ShuinDepartment of Urology, School of Medicine, Kochi University, Kochi 783-8505, Japan.
Tsuneharu MikiDepartment of Urology, Kyoto Prefectural University of Medicine, Kyoto 602-8566, Japan.
Koichi MatsudaLaboratory of Molecular Medicine, Human Genome Center, Institute of Medical Science, University of Tokyo, Tokyo 108-8639, Japan.
Yusuke NakamuraLaboratory of Molecular Medicine, Human Genome Center, Institute of Medical Science, University of Tokyo, Tokyo 108-8639, Japan.
Kyoto Prefectural University of Medicine · JPUniversity of Kochi · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In order to identify genes involved in renal carcinogenesis, we analyzed the expression profile of renal cell carcinomas (RCCs) using microarrays consisting of 27,648 cDNA or ESTs, and found a small heat shock protein, HSPB7, to be significantly and commonly downregulated in RCC. Subsequent quantitative PCR (qPCR) and immunohistochemical (IHC) analyses confirmed the downregulation of HSPB7 in RCC tissues and cancer cell lines in both transcriptional and protein levels. Bisulfite sequencing of a genomic region of HSPB7 detected DNA hypermethylation of some segments of HSPB7 in RCC cells and concordantly 5-aza-2'-deoxycytidine (5-Aza-dC) treatment of cancer cells restored HSPB7 expression significantly. Ectopic introduction of HSPB7 in five RCC cell lines remarkably suppressed cancer cell growth. Interestingly, we found that HSPB7 expression could be induced by p53 in a dose-dependent manner, indicating that this gene functions in the p53 pathway. Our results imply that HSBP7 is likely to be a tumor suppressor gene regulated by p53 and its downregulation by hypermethylation may play a critical role in renal carcinogenesis.

Indexed as

DNA MethylationAntineoplastic AgentsAzacitidineBase SequenceCarcinoma, Renal CellCell Line, TumorDecitabineEpigenesis, GeneticGene Expression Regulation, NeoplasticHEK293 CellsHSP27 Heat-Shock ProteinsHumansKidney NeoplasmsMolecular Sequence DataOligonucleotide Array Sequence AnalysisSignal TransductionAntineoplastic AgentsAzacitidineDecitabineHSP27 Heat-Shock ProteinsHSPB7 protein, humanTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID24585183
PMCPMC4027944
OpenAlexW2056937266

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.