Evidence map›Paper›PMID 34030133›Full record

ArticleAging2021

NUPR1 is a novel potential biomarker and confers resistance to sorafenib in clear cell renal cell carcinoma by increasing stemness and targeting the PTEN/AKT/mTOR pathway.

Wei He, Fajuan Cheng, Bin Zheng, Jianwei Wang, Guiting Zhao, Zhongshun Yao, Tong Zhang

Open access · hybridAbstract read
In one paragraph

Article in Aging, 2021. 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
2.1field-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

15 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
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  10. [Mechanism of nuclear protein 1 in the resistance to axitinib in clear cell renal cell carcinoma].Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences · 2023
    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.

Wei HeDepartment of Urology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, China.
Fajuan ChengDepartment of Nephrology, Shandong Provincial Hospital Affiliated to Shandong University, Jinan, Shandong, China.
Bin ZhengDepartment of Urology, Shandong Provincial Hospital, Cheeloo College of Medicine, Shandong University, Jinan, Shandong, China.
Jianwei WangDepartment of Urology, Shandong Provincial ENT Hospital Affiliated to Shandong University, Jinan, Shandong, China.
Guiting ZhaoDepartment of Urology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, China.
Zhongshun YaoDepartment of Urology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, China.
Tong ZhangDepartment of Urology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, China.
Shandong Provincial Hospital · CNShandong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSorafenib can improve the survival of metastatic clear cell renal cell carcinoma (ccRCC) patients. However, its benefits are modest, as patients eventually become resistant, and the mechanisms remain elusive. NUPR1, a stress-induced protein, has been reported in malignancies and functions as an oncogene by modulating the stress response, facilitating survival in harsh environments and conferring drug resistance. However, its role in ccRCC has not been explored.

methodsThe expression and clinical significance of NUPR1 were analyzed in ccRCC patients in in-house patients and The Cancer Genome Atlas (TCGA) cohorts. The biological functions of NUPR1 were investigated. Xenografts were performed to confirm the effects of NUPR1 on tumorigenesis. The molecular mechanism of NUPR1 was investigated

resultsNUPR1 expression was upregulated in tumor tissue. Further analysis showed that NUPR1 overexpression was associated with an aggressive phenotype and predicted a poor prognosis. Depletion of NUPR1 suppressed tumorigenesis and sensitized cells to sorafenib treatment. Finally, mechanistic investigations indicated that NUPR1 promoted tumorigenesis in ccRCC by increasing stemness and activating the PTEN/AKT/mTOR signaling pathway.

conclusionsCollectively, our results suggest that NUPR1 may serve as a predictor of ccRCC. Notably, NUPR1 silencing reversed sorafenib resistance in ccRCC. These findings provide a novel potential therapeutic target in the clinical management of ccRCC.

Indexed as

Drug Resistance, NeoplasmSignal TransductionAgedAnimalsApoptosisBasic Helix-Loop-Helix ProteinsBiomarkers, TumorCarcinoma, Renal CellCell Cycle CheckpointsCell Line, TumorCell ProliferationDisease-Free SurvivalDown-RegulationFemaleGene Expression Regulation, NeoplasticHumansBasic Helix-Loop-Helix ProteinsBiomarkers, TumorNeoplasm ProteinsNUPR1 protein, humanProto-Oncogene Proteins c-aktPTEN PhosphohydrolaseSorafenibTOR Serine-Threonine Kinasesclear cell renal cell carcinomamTORNUPR1stemnesstherapy resistance

Identifiers

PMID34030133
PMCPMC8202846
OpenAlexW3165549650

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.