Evidence map›Paper›PMID 23376929›Full record

ArticleNucleic acids research2013

Transcribed pseudogene ψPPM1K generates endogenous siRNA to suppress oncogenic cell growth in hepatocellular carcinoma.

Wen-Ling Chan, Chung-Yee Yuo, Wen-Kuang Yang, Shih-Ya Hung, Ya-Sian Chang, Chien-Chih Chiu, Kun-Tu Yeh, Hsien-Da Huang, Jan-Gowth Chang

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 1 pooled it
3.4field-weighted citation impact, top 7% 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

42 citing papers in PubMed, 1 synthesis or guideline pooled it, 69 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Review
  5. Article
  6. The NIMA-related kinase family and cancer.Frontiers in oncology · 2025
    Review
  7. Article
  8. Review
  9. In Mitosis You Are Not: The NIMA Family of Kinases inInternational journal of molecular sciences · 2022
    Review
  10. Article
  11. Article
  12. Pseudogenes as Biomarkers and Therapeutic Targets in Human Cancers.Methods in molecular biology (Clifton, N.J.) · 2021
    Review
  13. Article
  14. Pseudogenes: Four Decades of Discovery.Methods in molecular biology (Clifton, N.J.) · 2021
    Article
  15. Identification of Potential Diagnostic and Prognostic Pseudogenes in Hepatocellular Carcinoma Based on Pseudogene-miRNA-mRNA Competitive Network.Medical science monitor : international medical journal of experimental and clinical research · 2020
    Article
  16. Review
  17. Article
  18. Review
  19. Article
  20. Article
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

9 authors at 2 institutions in 1 country.

Wen-Ling ChanInstitute of Bioinformatics and Systems Biology, National Chiao Tung University, Hsin-Chu 300, Taiwan.
Chung-Yee Yuo
Wen-Kuang Yang
Shih-Ya Hung
Ya-Sian Chang
Chien-Chih Chiu
Kun-Tu Yeh
Hsien-Da Huang
Jan-Gowth Chang
Kaohsiung Medical University · TWNational Yang Ming Chiao Tung University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pseudogenes, especially those that are transcribed, may not be mere genomic fossils, but their biological significance remains unclear. Postulating that in the human genome, as in animal models, pseudogenes may function as gene regulators through generation of endo-siRNAs (esiRNAs), antisense RNAs or RNA decoys, we performed bioinformatic and subsequent experimental tests to explore esiRNA-mediated mechanisms of pseudogene involvement in oncogenesis. A genome-wide survey revealed a partial retrotranscript pseudogene ψPPM1K containing inverted repeats capable of folding into hairpin structures that can be processed into two esiRNAs; these esiRNAs potentially target many cellular genes, including NEK8. In 41 paired surgical specimens, we found significantly reduced expression of two predicted ψPPM1K-specific esiRNAs, and the cognate gene PPM1K, in hepatocellular carcinoma compared with matched non-tumour tissues, whereas the expression of target gene NEK8 was increased in tumours. Additionally, NEK8 and PPM1K were downregulated in stably transfected ψPPM1K-overexpressing cells, but not in cells transfected with an esiRNA1-deletion mutant of ψPPM1K. Furthermore, expression of NEK8 in ψPPM1K-transfected cells demonstrated that NEK8 can counteract the growth inhibitory effects of ψPPM1K. These findings indicate that a transcribed pseudogene can exert tumour-suppressor activity independent of its parental gene by generation of esiRNAs that regulate human cell growth.

Indexed as

Gene Expression Regulation, NeoplasticPseudogenesBase SequenceCarcinoma, HepatocellularCell Line, TumorCell ProliferationCell Transformation, NeoplasticDown-RegulationHumansLiver NeoplasmsMicroRNAsMitochondriaMolecular Sequence DataNIMA-Related KinasesPhosphoprotein PhosphatasesProtein KinasesMicroRNAsNEK8 protein, humanNIMA-Related KinasesPhosphoprotein PhosphatasesPPM1K protein, humanProtein KinasesProtein Phosphatase 2CRNA PrecursorsRNA, Small Interfering

Identifiers

PMID23376929
PMCPMC3616710
OpenAlexW2165782989

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.