Evidence map›Paper›PMID 31581360›Full record

ArticleMolecular oncology2019

MiR-195 and miR-497 suppress tumorigenesis in lung cancer by inhibiting SMURF2-induced TGF-β receptor I ubiquitination.

Dong-Kyu Chae, Jinyoung Park, Moonsoo Cho, Eunmi Ban, Mihue Jang, Young Sook Yoo, Eunice EunKyeong Kim, Ja-Hyun Baik, Eun Joo Song

Abstract read
In one paragraph

Article in Molecular oncology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
–field-weighted citation impact
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

45 citing papers in PubMed.

  1. SMURF2 in Anticancer Therapy: Dual Role in Carcinogenesis and Theranostics.International journal of molecular sciences · 2026
    Review
  2. Article
  3. Review
  4. Article
  5. The role of microRNAs in calcific aortic valve disease.Frontiers in cardiovascular medicine · 2025
    Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Annals of translational medicine · 2022
    Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review
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.

Dong-Kyu ChaeMolecular Recognition Research Center, Korea Institute of Science and Technology, Seoul, Korea.
Jinyoung ParkMolecular Recognition Research Center, Korea Institute of Science and Technology, Seoul, Korea.
Moonsoo ChoMolecular Recognition Research Center, Korea Institute of Science and Technology, Seoul, Korea.
Eunmi BanMolecular Recognition Research Center, Korea Institute of Science and Technology, Seoul, Korea.
Mihue JangBiomedical Research Institute, Korea Institute of Science and Technology, Seoul, Korea.ORCID 0000-0002-2135-2983
Young Sook YooMolecular Recognition Research Center, Korea Institute of Science and Technology, Seoul, Korea.
Eunice EunKyeong KimBiomedical Research Institute, Korea Institute of Science and Technology, Seoul, Korea.
Ja-Hyun BaikSchool of Life Sciences and Biotechnology, Korea University, Seoul, Korea.
Eun Joo SongGraduate School of Pharmaceutical Sciences and College of Pharmacy, Ewha Womans University, Seoul, Korea.ORCID 0000-0002-2420-6666

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

SMURF2 is a member of the HECT family of E3 ubiquitin ligases that have important roles as a negative regulator of transforming growth factor-β (TGF-β) signaling through ubiquitin-mediated degradation of TGF-β receptor I. However, the regulatory mechanism of SMURF2 is largely unknown. In this study, we identified that micro(mi)R-195 and miR-497 putatively target SMURF2 using several target prediction databases. Both miR-195 and miR-497 bind to the 3'-UTR of the SMURF2 mRNA and inhibit SMURF2 expression. Furthermore, miR-195 and miR-497 regulate SMURF2-dependent TβRI ubiquitination and cause the activation of the TGF-β signaling pathway in lung cancer cells. Upregulation of miR-195 and miR-497 significantly reduced cell viability and colony formation through the activation of TGF-β signaling. Interestingly, miR-195 and miR-497 also reduced the invasion ability of lung cancer cells when cells were treated with TGF-β1. Subsequent in vivo studies in xenograft nude mice model revealed that miR-195 and miR-497 repress tumor growth. These findings demonstrate that miR-195 and miR-497 act as a tumor suppressor by suppressing ubiquitination-mediated degradation of TGF-β receptors through SMURF2, and suggest that miR-195 and miR-497 are potential therapeutic targets for lung cancer.

Indexed as

CarcinogenesisGenes, Tumor SuppressorLung NeoplasmsMicroRNAsNeoplasm ProteinsReceptor, Transforming Growth Factor-beta Type IRNA, NeoplasmUbiquitin-Protein LigasesA549 CellsAnimalsFemaleHumansMiceMice, NudeUbiquitinationMicroRNAsMIRN195 microRNA, humanMIRN497 microRNA, humanNeoplasm ProteinsReceptor, Transforming Growth Factor-beta Type IRNA, NeoplasmSMURF2 protein, humanTGFBR1 protein, humanUbiquitin-Protein Ligaseslung cancermiR-195miR-497SMURF2Transforming growth factor (TGF)-β

Identifiers

PMID31581360
PMCPMC6887584

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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.