Evidence map›Paper›PMID 35562668›Full record

ArticleCellular & molecular biology letters2022

RNF7 inhibits apoptosis and sunitinib sensitivity and promotes glycolysis in renal cell carcinoma via the SOCS1/JAK/STAT3 feedback loop.

Chengwu Xiao, Wei Zhang, Meimian Hua, Huan Chen, Bin Yang, Ye Wang, Qing Yang

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

Article in Cellular & molecular biology letters, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.6field-weighted citation impact, top 9% 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

15 citing papers in PubMed, 21 citations in OpenAlex.

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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.

Chengwu XiaoDepartment of Urology, Changhai Hospital, Naval Medical University, No. 168 Changhai Road, Yangpu, Shanghai, 200433, China.
Wei ZhangDepartment of Urology, Changhai Hospital, Naval Medical University, No. 168 Changhai Road, Yangpu, Shanghai, 200433, China.
Meimian HuaDepartment of Urology, Changhai Hospital, Naval Medical University, No. 168 Changhai Road, Yangpu, Shanghai, 200433, China.
Huan ChenDepartment of Urology, Changhai Hospital, Naval Medical University, No. 168 Changhai Road, Yangpu, Shanghai, 200433, China.
Bin YangDepartment of Urology, Changhai Hospital, Naval Medical University, No. 168 Changhai Road, Yangpu, Shanghai, 200433, China.
Ye WangDepartment of Urology, Changhai Hospital, Naval Medical University, No. 168 Changhai Road, Yangpu, Shanghai, 200433, China.
Qing YangDepartment of Urology, Changhai Hospital, Naval Medical University, No. 168 Changhai Road, Yangpu, Shanghai, 200433, China. yangqchsmmu@163.com.
Second Military Medical University · CNChanghai Hospital · CN

Funding

Precision Good Clinical Practice Center For Novel Drugs of Tumor and Diseases of Genitourinary System 2017ZX09304030Shanghai Clinical Medical Center of Urological Diseases Program 2017ZZ01005
6 · The paper itself

Abstract

backgroundRING finger protein 7 (RNF7) is a highly conserved protein that functions as an E3 ubiquitin ligase. RNF7 overexpression is indicated in multiple human cancers, but its role in renal cell carcinoma (RCC) and the mechanisms underlying how it regulates the initiation and progression of RCC have not been explored.

methodsBioinformatics analysis, quantitative reverse-transcription polymerase chain reaction (RT-PCR), and Western blot were conducted to determine the expression of RNF7 in RCC tissues and cell lines. Knockdown and overexpression experiments were performed to examine the effects of RNF7 on cell viability, apoptosis, and glycolysis in vitro and on tumor growth in nude mice in vivo.

resultsThe elevated RNF7 expression in tumor tissues of patients with RCC was correlated with poor survival. RNF7 overexpression inhibited apoptosis and promoted glycolysis in vitro and increased tumor growth in vivo by activating the JAK/STAT3 signaling pathway by ubiquitination of SOCS1. Moreover, RNF7 overexpression affected the sensitivity of RCC cells to sunitinib. Finally, STAT3 activation was necessary for transcriptional induction of RNF7.

conclusionThese results demonstrate that RNF7 inhibited apoptosis, promoted glycolysis, and inhibited sunitinib sensitivity in RCC cells via ubiquitination of SOCS1, thus activating STAT3 signaling. These suggest the potential for targeting the RNF7-SOCS1/JAK/STAT3 pathway for RCC treatment.

Indexed as

Carcinoma, Renal CellKidney NeoplasmsAnimalsApoptosisCell Line, TumorCell ProliferationFeedback, PhysiologicalGene Expression Regulation, NeoplasticGlycolysisHumansMaleMiceMice, NudeSTAT3 Transcription FactorSunitinibSuppressor of Cytokine Signaling 1 ProteinRNF7 protein, humanSOCS1 protein, humanSocs1 protein, mouseSTAT3 protein, humanSTAT3 Transcription FactorSunitinibSuppressor of Cytokine Signaling 1 ProteinSuppressor of Cytokine Signaling ProteinsUbiquitin-Protein LigasesApoptosisClear cell renal cell carcinomaGlycolysisJAK/STAT3RNF7SOCS1

Identifiers

PMID35562668
PMCPMC9107170
OpenAlexW4280622773

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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.