Evidence map›Paper›PMID 25997740›Full record

ArticleMolecules and cells2015

miR-335 Targets SIAH2 and Confers Sensitivity to Anti-Cancer Drugs by Increasing the Expression of HDAC3.

Youngmi Kim, Hyuna Kim, Deokbum Park, Dooil Jeoung

Open access · diamondAbstract read
In one paragraph

Article in Molecules and cells, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

25 citing papers in PubMed, 42 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Functions and Targets of miR-335 in Cancer.OncoTargets and therapy · 2021
    Review
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Aging · 2019
    Article
  16. Role of HDAC3-miRNA-CAGE Network in Anti-Cancer Drug-Resistance.International journal of molecular sciences · 2018
    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

4 authors at 1 institution in 1 country.

Youngmi KimDepartment of Biochemistry, College of Natural Sciences, Kangwon National University, Chunchon 200-701, Korea.
Hyuna KimDepartment of Biochemistry, College of Natural Sciences, Kangwon National University, Chunchon 200-701, Korea.
Deokbum ParkDepartment of Biochemistry, College of Natural Sciences, Kangwon National University, Chunchon 200-701, Korea.
Dooil JeoungDepartment of Biochemistry, College of Natural Sciences, Kangwon National University, Chunchon 200-701, Korea.
Kangwon National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We previously reported the role of histone deacetylase 3 (HDAC3) in response to anti-cancer drugs. The decreased expression of HDAC3 in anti-cancer drug-resistant cancer cell line is responsible for the resistance to anti-cancer drugs. In this study, we investigated molecular mechanisms associated with regulation of HDAC3 expression. MG132, an inhibitor of proteasomal degradation, induced the expression of HDAC3 in various anti-cancer drug-resistant cancer cell lines. Ubiquitination of HDAC3 was observed in various anti-cancer drug-resistant cancer cell lines. HDAC3 showed an interaction with SIAH2, an ubiquitin E3 ligase, that has increased expression in various anti-cancer drug-resistant cancer cell lines. miRNA array analysis showed the decreased expression of miR-335 in these cells. Targetscan analysis predicted the binding of miR-335 to the 3'-UTR of SIAH2. miR-335-mediated increased sensitivity to anti-cancer drugs was associated with its effect on HDAC3 and SIAH2 expression. miR-335 exerted apoptotic effects and inhibited ubiquitination of HDAC3 in anti-cancer drug-resistant cancer cell lines. miR-335 negatively regulated the invasion, migration, and growth rate of cancer cells. The mouse xenograft model showed that miR-335 negatively regulated the tumorigenic potential of cancer cells. The down-regulation of SIAH2 conferred sensitivity to anti-cancer drugs. The results of the study indicated that the miR-335/SIAH2/HDAC3 axis regulates the response to anti-cancer drugs.

Indexed as

AnimalsCell Line, TumorDrug Resistance, NeoplasmFemaleHeterograftsHistone Deacetylase 3Histone DeacetylasesHumansLeupeptinsMiceMice, Inbred BALB CMice, NudeMicroRNAsNuclear ProteinsSeven in Absentia ProteinsUbiquitin-Protein Ligasesbenzyloxycarbonylleucyl-leucyl-leucine aldehydeHistone Deacetylase 3Histone DeacetylasesLeupeptinsMicroRNAsMIRN335 microRNA, humanNuclear ProteinsSeven in Absentia ProteinsUbiquitin-Protein Ligasesanti-cancer drug-resistancemiR-335SIAH2ubiquitination

Identifiers

PMID25997740
PMCPMC4469914
OpenAlexW2398951825

What OpenQuestion holds

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LicenceCC BY-NC-SA
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.