Evidence map›Paper›PMID 35034103›Full record

ArticleCell death and differentiation2022

Non-coding small nucleolar RNA SNORD17 promotes the progression of hepatocellular carcinoma through a positive feedback loop upon p53 inactivation.

Junnan Liang, Ganxun Li, Jingyu Liao, Zhao Huang, Jingyuan Wen, Yu Wang, Zeyu Chen, Guangzhen Cai, Weiqi Xu, Zeyang Ding and 5 more

Open access · bronzeAbstract read
In one paragraph

Article in Cell death and differentiation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
6.1field-weighted citation impact, top 2% 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

43 citing papers in PubMed, 66 citations in OpenAlex.

  1. Review
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  10. Review
  11. Chemically modified non-coding RNAs in cancer.Expert reviews in molecular medicine · 2025
    Review
  12. Article
  13. Article
  14. Small nucleolar RNAs: the hidden precursors of cancer ribosomes.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2025
    Review
  15. Article
  16. Article
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  18. Review
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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

15 authors at 4 institutions in 2 countries.

Junnan Liang *Hepatic Surgery Center, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Ganxun Li *Hepatic Surgery Center, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Jingyu Liao *Hepatic Surgery Center, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.ORCID http://orcid.org/0000-0002-4522-0651
Zhao Huang *Hepatic Surgery Center, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Jingyuan WenHepatic Surgery Center, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Yu WangHepatic Surgery Center, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Zeyu ChenHepatic Surgery Center, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Guangzhen CaiHepatic Surgery Center, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Weiqi XuHepatic Surgery Center, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Zeyang DingHepatic Surgery Center, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Huifang LiangHepatic Surgery Center, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.ORCID http://orcid.org/0000-0001-6874-3634
Pran K DattaDivision of Hematology and Oncology, Department of Medicine, UAB Comprehensive Cancer Center, Birmingham, AL, USA.
Liang ChuHepatic Surgery Center, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. Liangchu@tjh.tjmu.edu.cn.ORCID http://orcid.org/0000-0001-9209-2181
Xiaoping ChenHepatic Surgery Center, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. chenxpchenxp@163.com.ORCID http://orcid.org/0000-0001-8636-0493
Bixiang ZhangHepatic Surgery Center, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. bixiangzhang@163.com.ORCID http://orcid.org/0000-0002-8546-7472
Tongji Hospital · CNMinistry of Education of the People's Republic of China · CNHubei Provincial Women and Children's Hospital · CNSylvester Comprehensive Cancer Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent evidence suggests that small nucleolar RNAs (snoRNAs) are involved in the progression of various cancers, but their precise roles in hepatocellular carcinoma (HCC) remain largely unclear. Here, we report that SNORD17 promotes the progression of HCC through a positive feedback loop with p53. HCC-related microarray datasets from the Gene Expression Omnibus (GEO) database and clinical HCC samples were used to identify clinically relevant snoRNAs in HCC. SNORD17 was found upregulated in HCC tissues compared with normal liver tissues, and the higher expression of SNORD17 predicted poor outcomes in patients with HCC, especially in those with wild-type p53. SNORD17 promoted the growth and tumorigenicity of HCC cells in vitro and in vivo by inhibiting p53-mediated cell cycle arrest and apoptosis. Mechanistically, SNORD17 anchored nucleophosmin 1 (NPM1) and MYB binding protein 1a (MYBBP1A) in the nucleolus by binding them simultaneously. Loss of SNORD17 promoted the translocation of NPM1 and MYBBP1A into the nucleoplasm, leading to NPM1/MDM2-mediated stability and MYBBP1A/p300-mediated activation of p53. Interestingly, p300-mediated acetylation of p53 inhibited SNORD17 expression by binding to the promoter of SNORD17 in turn, forming a positive feedback loop between SNORD17 and p53. Administration of SNORD17 antisense oligonucleotides (ASOs) significantly suppressed the growth of xenograft tumors in mice. In summary, this study suggests that SNORD17 drives cancer progression by constitutively inhibiting p53 signaling in HCC and may represent a potential therapeutic target for HCC.

Indexed as

Carcinoma, HepatocellularLiver NeoplasmsRNA, Small NucleolarAnimalsCell Line, TumorCell ProliferationDNA-Binding ProteinsFeedbackGene Expression Regulation, NeoplasticHumansMiceNucleophosminRNA-Binding ProteinsTranscription FactorsTumor Suppressor Protein p53DNA-Binding ProteinsMYBBP1A protein, humanNPM1 protein, humanNucleophosminRNA-Binding ProteinsRNA, Small NucleolarTranscription FactorsTumor Suppressor Protein p53

Identifiers

PMID35034103
PMCPMC9090725
OpenAlexW4206002665

What OpenQuestion holds

Textmetadata
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.