Evidence map›Paper›PMID 32958058›Full record

ArticleJournal of experimental & clinical cancer research : CR2020

NUCKS promotes cell proliferation and suppresses autophagy through the mTOR-Beclin1 pathway in gastric cancer.

Erhu Zhao, Liying Feng, Longchang Bai, Hongjuan Cui

Open access · goldAbstract read
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
3.6field-weighted citation impact, top 6% 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

23 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
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  3. Targeting NUCKS1 with a fragment of tRNANon-coding RNA research · 2025
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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

4 authors at 2 institutions in 2 countries.

Erhu ZhaoState Key Laboratory of Silkworm Genome Biology, College of Biotechnology, Southwest University, No.2 Tiansheng Road, Beibei District, Chongqing, 400716, China.
Liying FengState Key Laboratory of Silkworm Genome Biology, College of Biotechnology, Southwest University, No.2 Tiansheng Road, Beibei District, Chongqing, 400716, China.
Longchang BaiState Key Laboratory of Silkworm Genome Biology, College of Biotechnology, Southwest University, No.2 Tiansheng Road, Beibei District, Chongqing, 400716, China.
Hongjuan CuiState Key Laboratory of Silkworm Genome Biology, College of Biotechnology, Southwest University, No.2 Tiansheng Road, Beibei District, Chongqing, 400716, China. hcui@swu.edu.cn.
Southwest University · CNState Key Laboratory of Silkworm Genomic Biology

Funding

Chongqing University Innovation Team Building Program funded projects CXTDX201601010National Key Research and Development Program of China 2016YFC1302204National Natural Science Foundation of China 81872071National Natural Science Foundation of China 81972357Natural Science Foundation of Chongqing cstc2018jcyjAX0330Natural Science Foundation of Chongqing cstc2019jcyj-zdxmX0033
6 · The paper itself

Abstract

backgroundNuclear casein kinase and cyclin-dependent kinase substrate (NUCKS), a novel gene first reported in 2001, is a member of the high mobility group (HMG) family. Although very little is known regarding the biological roles of NUCKS, emerging clinical evidence suggests that the NUCKS protein can be used as a biomarker and therapeutic target in various human ailments, including several types of cancer.

methodsWe first assessed the potential correlation between NUCKS expression and gastric cancer prognosis. Then functional experiments were conducted to evaluate the effects of NUCKS in cell proliferation, cell cycle, apoptosis and autophagy. Finally, the roles of NUCKS on gastric cancer were examined in vivo.

resultsWe found that NUCKS was overexpressed in gastric cancer patients with poor prognosis. Through manipulating NUCKS expression, it was observed to be positively associated with cell proliferation in vitro and in vivo. NUCKS knockdown could induce cell cycle arrest and apoptosis. Then further investigation indicated that NUCKS knockdown could also significantly induce a marked increase in autophagy though the mTOR-Beclin1 pathway, which could be was rescued by NUCKS restoration. Moreover, silencing Beclin1 in NUCKS knockdown cells or adding rapamycin in NUCKS-overexpressed cells also confirmed these results.

conclusionsOur findings revealed that NUCKS functions as an oncogene and an inhibitor of autophagy in gastric cancer. Thus, the downregulation or inhibition of NUCKS may be a potential therapeutic strategy for gastric cancer.

Indexed as

AnimalsAutophagyBeclin-1CarcinogenesisCell Line, TumorCell ProliferationDisease-Free SurvivalFemaleHeterograftsHumansKaplan-Meier EstimateMaleMiceNuclear ProteinsPhosphoproteinsSignal TransductionBeclin-1MTOR protein, humanNUCKS1 protein, humanNuclear ProteinsPhosphoproteinsTOR Serine-Threonine KinasesAutophagyBeclin1Gastric cancermTORNUCKS

Identifiers

PMID32958058
PMCPMC7504682
OpenAlexW3087312532

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.