Evidence map›Paper›PMID 29780166›Full record

ArticleOncogene2018

NUDT21 negatively regulates PSMB2 and CXXC5 by alternative polyadenylation and contributes to hepatocellular carcinoma suppression.

Sheng Tan, Hua Li, Weijie Zhang, Yunying Shao, Yuan Liu, Haiyang Guan, Jun Wu, Yani Kang, Junsong Zhao, Qing Yu and 11 more

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.

0numbers the graph read from it
0cells of the map it votes in
74citing papers in PubMed
6.7field-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

74 citing papers in PubMed, 121 citations in OpenAlex.

  1. Article
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  8. CXXC5 is a ubiquitinated protein and is degraded by the ubiquitin-proteasome pathway.Protein science : a publication of the Protein Society · 2025
    Article
  9. Article
  10. Characterization and molecular targeting of CFIm25 (NUDT21/CPSF5) mRNA using miRNAs.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
  11. Article
  12. Signal integrator function of CXXC5 in Cancer.Cell communication and signaling : CCS · 2025
    Review
  13. Review
  14. REMR: Identification of RNA Editing-mediated MiRNA Regulation in Cancers.Computational and structural biotechnology journal · 2024
    Article
  15. Article
  16. Article
  17. Article
  18. Article
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  20. Article

14 more citing papers are in PubMed but not listed here.

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

21 authors at 4 institutions in 1 country.

Sheng TanHefei National Laboratory for Physical Sciences at Microscale, the CAS Key Laboratory of Innate Immunity and Chronic Disease, School of Life Sciences, University of Science and Technology of China, Hefei, Anhui, 230027, China.
Hua LiSchool of Biomedical Engineering, Bio-ID Center, Shanghai Jiao Tong University, Shanghai, 200240, China.
Weijie ZhangHefei National Laboratory for Physical Sciences at Microscale, the CAS Key Laboratory of Innate Immunity and Chronic Disease, School of Life Sciences, University of Science and Technology of China, Hefei, Anhui, 230027, China.
Yunying ShaoHefei National Laboratory for Physical Sciences at Microscale, the CAS Key Laboratory of Innate Immunity and Chronic Disease, School of Life Sciences, University of Science and Technology of China, Hefei, Anhui, 230027, China.
Yuan LiuHefei National Laboratory for Physical Sciences at Microscale, the CAS Key Laboratory of Innate Immunity and Chronic Disease, School of Life Sciences, University of Science and Technology of China, Hefei, Anhui, 230027, China.
Haiyang GuanHefei National Laboratory for Physical Sciences at Microscale, the CAS Key Laboratory of Innate Immunity and Chronic Disease, School of Life Sciences, University of Science and Technology of China, Hefei, Anhui, 230027, China.
Jun WuSchool of Biomedical Engineering, Bio-ID Center, Shanghai Jiao Tong University, Shanghai, 200240, China.
Yani KangSchool of Biomedical Engineering, Bio-ID Center, Shanghai Jiao Tong University, Shanghai, 200240, China.
Junsong ZhaoHefei National Laboratory for Physical Sciences at Microscale, the CAS Key Laboratory of Innate Immunity and Chronic Disease, School of Life Sciences, University of Science and Technology of China, Hefei, Anhui, 230027, China.
Qing YuHefei National Laboratory for Physical Sciences at Microscale, the CAS Key Laboratory of Innate Immunity and Chronic Disease, School of Life Sciences, University of Science and Technology of China, Hefei, Anhui, 230027, China.
Yunzhao GuSchool of Biomedical Engineering, Bio-ID Center, Shanghai Jiao Tong University, Shanghai, 200240, China.
Keshuo DingDepartment of Pathology, Anhui Medical University, Meishan Road, Hefei, Anhui, 230031, China.
Min ZhangHefei National Laboratory for Physical Sciences at Microscale, the CAS Key Laboratory of Innate Immunity and Chronic Disease, School of Life Sciences, University of Science and Technology of China, Hefei, Anhui, 230027, China.
Wenchang QianHefei National Laboratory for Physical Sciences at Microscale, the CAS Key Laboratory of Innate Immunity and Chronic Disease, School of Life Sciences, University of Science and Technology of China, Hefei, Anhui, 230027, China.
Yong ZhuHefei National Laboratory for Physical Sciences at Microscale, the CAS Key Laboratory of Innate Immunity and Chronic Disease, School of Life Sciences, University of Science and Technology of China, Hefei, Anhui, 230027, China.
Huayong CaiHefei National Laboratory for Physical Sciences at Microscale, the CAS Key Laboratory of Innate Immunity and Chronic Disease, School of Life Sciences, University of Science and Technology of China, Hefei, Anhui, 230027, China.
Changyu ChenFirst Affiliated Hospital of Anhui Medical University, Anhui Medical University, Meishan Road, Hefei, Anhui, 230031, China.
Peter E LobieTsinghua-Berkeley Shenzhen Institute, Precision Medicine & Healthcare Research Center, Tsinghua University, Shenzhen, 518055, China.
Xiaodong ZhaoKey Laboratory of Systems Biomedicine (Ministry of Education), Shanghai Center for Systems Biomedicine, Shanghai Jiao Tong University, 800 Dongchuan Road, Shanghai, 200240, China. xiaodongzhao@sjtu.edu.cn.
Jielin SunKey Laboratory of Systems Biomedicine (Ministry of Education), Shanghai Center for Systems Biomedicine, Shanghai Jiao Tong University, 800 Dongchuan Road, Shanghai, 200240, China. jlsun@sjtu.edu.cn.
Tao ZhuHefei National Laboratory for Physical Sciences at Microscale, the CAS Key Laboratory of Innate Immunity and Chronic Disease, School of Life Sciences, University of Science and Technology of China, Hefei, Anhui, 230027, China. zhut@ustc.edu.cn.
University of Science and Technology of China · CNShanghai Jiao Tong University · CNAnhui Medical University · CNTsinghua University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alternative polyadenylation (APA) is an important post-transcriptional regulatory mechanism and involved in many diseases, including cancer. CFIm25, a subunit of the cleavage factor I encoded by NUDT21, is required for 3'RNA cleavage and polyadenylation. Although it has been recently reported to be involved in glioblastoma tumor suppression, its roles and the underlying functional mechanism remain unclear in other types of cancer. In this study, we characterized NUDT21 in hepatocellular carcinoma (HCC). Reduced expression of NUDT21 was observed in HCC tissue compared to adjacent non-tumorous compartment. HCC patients with lower NUDT21 expression have shorter overall and disease-free survival times than those with higher NUDT21 expression after surgery. Knockdown of NUDT21 promotes HCC cell proliferation, metastasis, and tumorigenesis, whereas forced expression of NUDT21 exhibits the opposite effects. We then performed global APA site profiling analysis in HCC cells and identified considerable number of genes with shortened 3'UTRs upon the modulation of NUDT21 expression. In particular, we further characterized the NUDT21-regulated genes PSMB2 and CXXC5. We found NUDT21 knockdown increases usage of the proximal polyadenylation site in the PSMB2 and CXXC5 3' UTRs, resulting in marked increase in the expression of PSMB2 and CXXC5. Moreover, knockdown of PSMB2 or CXXC5 suppresses HCC cell proliferation and invasion. Taken together, our study demonstrated that NUDT21 inhibits HCC proliferation, metastasis and tumorigenesis, at least in part, by suppressing PSMB2 and CXXC5, and thereby provided a new insight into understanding the connection of HCC suppression and APA machinery.

Indexed as

3' Untranslated RegionsAnimalsCarcinogenesisCarcinoma, HepatocellularCarrier ProteinsCell Line, TumorCell ProliferationCleavage And Polyadenylation Specificity FactorDisease-Free SurvivalDNA-Binding ProteinsGene Expression Regulation, NeoplasticHumansLiver NeoplasmsMaleMiceMice, Nude3' Untranslated RegionsCarrier ProteinsCleavage And Polyadenylation Specificity FactorCXXC5 protein, humanDNA-Binding ProteinsNudt21 protein, humanProteasome Endopeptidase ComplexPSMB2 protein, humanTranscription Factors

Identifiers

PMID29780166
OpenAlexW2804591825

What OpenQuestion holds

Textmetadata
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.