Evidence map›Paper›PMID 27741516›Full record

ArticleOncotarget2016

SENP1 promotes proliferation of clear cell renal cell carcinoma through activation of glycolysis.

Baijun Dong, Yujing Gao, Xunlei Kang, Hongchang Gao, Jin Zhang, Hua Guo, Mingjian J You, Wei Xue, Jinke Cheng, Yiran Huang

Open access · diamondAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.0field-weighted citation impact, top 24% 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

16 citing papers in PubMed, 26 citations in OpenAlex.

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  12. Noncovalent structure of SENP1 in complex with SUMO2.Acta crystallographica. Section F, Structural biology communications · 2019
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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

10 authors at 5 institutions in 2 countries.

Baijun DongDepartment of Urology, School of Medicine, Renji Hospital, Shanghai Jiao Tong University, Shanghai, China.
Yujing GaoKey Laboratory of Fertility Preservation and Maintenance of Ministry of Education, Department of Biochemistry and Molecular Biology, Ningxia Medical University, Yinchuan, Ningxia, China.
Xunlei KangDepartment of Biochemistry and Molecular Cell Biology, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Hongchang GaoSchool of Pharmacy, Wenzhou Medical College, Wenzhou, China.
Jin ZhangDepartment of Urology, School of Medicine, Renji Hospital, Shanghai Jiao Tong University, Shanghai, China.
Hua GuoDepartment of Hematopathology, University of Texas MD Anderson Cancer Center, Houston, USA.
Mingjian J YouDepartment of Hematopathology, University of Texas MD Anderson Cancer Center, Houston, USA.
Wei XueDepartment of Urology, School of Medicine, Renji Hospital, Shanghai Jiao Tong University, Shanghai, China.
Jinke ChengDepartment of Biochemistry and Molecular Cell Biology, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Yiran HuangDepartment of Urology, School of Medicine, Renji Hospital, Shanghai Jiao Tong University, Shanghai, China.
Shanghai Jiao Tong University · CNRenji Hospital · CNThe University of Texas MD Anderson Cancer Center · USNingxia Medical University · CNWenzhou Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Metabolic shift toward aerobic glycolysis is a fundamental element contributing to the development and progression of clear cell renal cell carcinoma (ccRCC). We and others previously observed enhanced glycolysis and diminished tricarboxylic acid (TCA) cycle activity in ccRCC tissue. Here, by integrated gene expression and metabolomic analyses of 36 matched pairs of tumor and adjacent normal tissues, we showed that expression of Sentrin/SUMO-specific protease 1 (SENP1) is positively associated with glycolysis levels in ccRCC. Moreover, SENP1 knockdown in RCC4/VHL cells downregulated expression of key glycolytic enzymes under normoxic and hypoxic conditions and inhibited cell proliferation under hypoxic conditions, possibly due to ineffective deSUMOylation and stablization of Hif-1α related to the SENP-1 deficiency. Finally, SENP1 expression correlated positively with tumor pathological grade and was an indicator of poor overall survival and advanced tumor progression in ccRCC. Altered VHL gene function is found in 60-90% ccRCC cases of ccRCC, but therapies targeting VHL-related signaling pathways have been ineffective, spurring exploration of alternative pathological signaling events. Our results provide a possible mechanistic explanation for the role of SENP1 in the initiation and development of ccRCC with normal VHL activity, and identifies SENP1 as a potential treatment target for the disease.

Indexed as

Cell ProliferationGlycolysisCarcinoma, Renal CellCell Line, TumorCysteine EndopeptidasesFemaleGene Expression Regulation, EnzymologicGene Expression Regulation, NeoplasticHumansHypoxia-Inducible Factor 1, alpha SubunitKaplan-Meier EstimateKidney NeoplasmsMaleMiddle AgedNeoplasm StagingProtein StabilityCysteine EndopeptidasesHIF1A protein, humanHypoxia-Inducible Factor 1, alpha SubunitSENP1 protein, humanVHL protein, humanVon Hippel-Lindau Tumor Suppressor Proteinclear cell renal cell carcinomaglycolysisHIF-1αSENP1

Identifiers

PMID27741516
PMCPMC5348332
OpenAlexW2530166021

What OpenQuestion holds

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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.