Evidence map›Paper›PMID 28493459›Full record

ArticleAging cell2017

Enhanced NOLC1 promotes cell senescence and represses hepatocellular carcinoma cell proliferation by disturbing the organization of nucleolus.

Fuwen Yuan, Yu Zhang, Liwei Ma, Qian Cheng, Guodong Li, Tanjun Tong

Open access · goldAbstract read
In one paragraph

Article in Aging cell, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

33 citing papers in PubMed, 69 citations in OpenAlex.

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  8. American journal of cancer research · 2024
    Article
  9. Article
  10. Roles of NOLC1 in cancers and viral infection.Journal of cancer research and clinical oncology · 2023
    Review
  11. Neuroprotective Effect of α-Lipoic Acid against AβMolecules (Basel, Switzerland) · 2023
    Article
  12. Article
  13. 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

6 authors at 2 institutions in 1 country.

Fuwen YuanPeking University Research Center on Aging, Department of Biochemistry and Molecular Biology, Peking University Health Science Center, Beijing, Key Laboratory of Protein Posttranslational Modifications and Cell Function, Beijing, 100191, China.
Yu ZhangPeking University Research Center on Aging, Department of Biochemistry and Molecular Biology, Peking University Health Science Center, Beijing, Key Laboratory of Protein Posttranslational Modifications and Cell Function, Beijing, 100191, China.
Liwei MaPeking University Research Center on Aging, Department of Biochemistry and Molecular Biology, Peking University Health Science Center, Beijing, Key Laboratory of Protein Posttranslational Modifications and Cell Function, Beijing, 100191, China.
Qian ChengPeking University Research Center on Aging, Department of Biochemistry and Molecular Biology, Peking University Health Science Center, Beijing, Key Laboratory of Protein Posttranslational Modifications and Cell Function, Beijing, 100191, China.
Guodong LiPeking University Research Center on Aging, Department of Biochemistry and Molecular Biology, Peking University Health Science Center, Beijing, Key Laboratory of Protein Posttranslational Modifications and Cell Function, Beijing, 100191, China.
Tanjun TongPeking University Research Center on Aging, Department of Biochemistry and Molecular Biology, Peking University Health Science Center, Beijing, Key Laboratory of Protein Posttranslational Modifications and Cell Function, Beijing, 100191, China.
Peking University · CNPeking University Cancer Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The nucleolus is a key organelle that is responsible for the synthesis of rRNA and assembly of ribosomal subunits, which is also the center of metabolic control because of the critical role of ribosomes in protein synthesis. Perturbations of rRNA biogenesis are closely related to cell senescence and tumor progression; however, the underlying molecular mechanisms are not well understood. Here, we report that cellular senescence-inhibited gene (CSIG) knockdown up-regulated NOLC1 by stabilizing the 5'UTR of NOLC1 mRNA, and elevated NOLC1 induced the retention of NOG1 in the nucleolus, which is responsible for rRNA processing. Besides, the expression of NOLC1 was negatively correlated with CSIG in the aged mouse tissue and replicative senescent 2BS cells, and the down-regulation of NOLC1 could rescue CSIG knockdown-induced 2BS senescence. Additionally, NOLC1 expression was decreased in human hepatocellular carcinoma (HCC) tissue, and the ectopic expression of NOLC1 repressed the proliferation of HCC cells and tumor growth in a HCC xenograft model.

Indexed as

Gene Expression Regulation, Neoplastic5' Untranslated RegionsAgingAnimalsCarcinoma, HepatocellularCell Line, TumorCell NucleolusCell ProliferationCellular SenescenceFibroblastsGTP PhosphohydrolasesHEK293 CellsHumansLiver NeoplasmsMiceMice, Inbred BALB C5' Untranslated RegionsGTP PhosphohydrolasesNog1 protein, mouseNolc1 protein, mouseNuclear ProteinsPhosphoproteinsRibosomal ProteinsRNA, RibosomalRNA, Small InterferingagingCSIGhepatocellular carcinomaNOLC1nucleolus

Identifiers

PMID28493459
PMCPMC5506443
OpenAlexW2613910227

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.