Evidence map›Paper›PMID 28404905›Full record

ArticleOncotarget2017

OSR1 is a novel epigenetic silenced tumor suppressor regulating invasion and proliferation in renal cell carcinoma.

Yixiang Zhang, Yeqing Yuan, Pei Liang, Xiaojing Guo, Ying Ying, Xing-Sheng Shu, Michael Gao, Yingduan Cheng

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

22 citing papers in PubMed, 52 citations in OpenAlex.

  1. Nutrients · 2026
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  11. Osr1 regulates hepatic inflammation and cell survival in the progression of non-alcoholic fatty liver disease.Laboratory investigation; a journal of technical methods and pathology · 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

8 authors at 5 institutions in 2 countries.

Yixiang ZhangDepartment of Urology, The Second Affiliated Hospital of Jinan University, Shenzhen People's Hospital, Shenzhen, Guangdong, China.
Yeqing YuanDepartment of Urology, The Second Affiliated Hospital of Jinan University, Shenzhen People's Hospital, Shenzhen, Guangdong, China.
Pei LiangDepartment of Urology, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California, USA.
Xiaojing GuoDepartment of Pathology, The Second Affiliated Hospital of Jinan University, Shenzhen People's Hospital, Shenzhen, Guangdong, China.
Ying YingDepartment of Physiology, School of Basic Medical Sciences, Shenzhen University Health Sciences Center, Shenzhen, China.
Xing-Sheng ShuInstitute of Molecular Medicine, Health Science Center, Shenzhen University, Shenzhen, China.
Michael GaoDepartment of Urology, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California, USA.
Yingduan ChengTwigbiotechnology, Shenzhen, Guangdong, China.
Jinan University · CNShenzhen University Health Science Center · CNUniversity of California, Los Angeles · USBGI Group (China) · CNShenzhen Second People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Renal cell carcinoma (RCC) is one of the most malignant tumors in human. Here, we found that odd-skipped related transcription factor 1 (OSR1) was downregulated in 769-P and 786-O cells due to promoter CpG methylation. OSR1 expression could be restored by pharmacological demethylation treatment in silenced cell lines. Knockdown of OSR1 in two normal expressed cell lines- A498 and ACHN promoted cell invasion and cellular proliferation. RNA-Sequencing analysis showed that expression profile of genes involved in multiple cancer-related pathways was changed when OSR1 was downregulated. By quantitative real-time PCR, we confirmed that depletion of OSR1 repressed the expression of several tumor suppresor genes involved in p53 pathway, such as p53, p21, p27, p57 and RB in A498 and ACHN. Moreover, knockdown of OSR1 suppressed the transcriptional activity of p53. Of note, OSR1 depletion also led to increased expression of a few oncogenic genes. We further evaluated the clinical significance of OSR1 in primary human RCC specimens by immunohistochemical staining and found that OSR1 expression was downregulated in primary RCC and negatively correlated with histological grade. Thus, our data indicate that OSR1 is a novel tumor suppressor gene in RCC. Downregulation of OSR1 might represent a potentially prognostic marker and therapeutic target for RCC.

Indexed as

Epigenesis, GeneticGene SilencingGenes, Tumor SuppressorAdultAgedCarcinoma, Renal CellCell Line, TumorCell MovementCell ProliferationDNA MethylationFemaleGene Expression ProfilingGene Expression Regulation, NeoplasticHumansKidney NeoplasmsMaleOSR1 protein, humanTranscription FactorsinvasionmethylationOSR1proliferationRCC

Identifiers

PMID28404905
PMCPMC5444721
OpenAlexW2590594464

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.