Evidence map›Paper›PMID 30589909›Full record

ArticlePloS one2018

MicroRNA-8073: Tumor suppressor and potential therapeutic treatment.

Atsuko Mizoguchi, Aiko Takayama, Taiga Arai, Junpei Kawauchi, Hiroko Sudo

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.1field-weighted citation impact, top 26% 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

21 citing papers in PubMed, 27 citations in OpenAlex.

  1. Review
  2. Microrna Expression inMicroRNA (Shariqah, United Arab Emirates) · 2026
    Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Review
  11. The Role of MiRNA in Cancer: Pathogenesis, Diagnosis, and Treatment.Methods in molecular biology (Clifton, N.J.) · 2022
    Article
  12. Review
  13. Review
  14. MicroRNA-Based Therapeutics for Drug-Resistant Colorectal Cancer.Pharmaceuticals (Basel, Switzerland) · 2021
    Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Review
  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

5 authors at 1 institution in 1 country.

Atsuko MizoguchiNew Frontiers Research Laboratories, Toray Industries, Inc., Kamakura, Kanagawa, Japan.ORCID 0000-0002-9389-5709
Aiko TakayamaNew Frontiers Research Laboratories, Toray Industries, Inc., Kamakura, Kanagawa, Japan.ORCID 0000-0003-4745-052X
Taiga AraiNew Frontiers Research Laboratories, Toray Industries, Inc., Kamakura, Kanagawa, Japan.ORCID 0000-0003-3249-612X
Junpei KawauchiNew Frontiers Research Laboratories, Toray Industries, Inc., Kamakura, Kanagawa, Japan.
Hiroko SudoNew Frontiers Research Laboratories, Toray Industries, Inc., Kamakura, Kanagawa, Japan.
Toray Industries, Inc. (Japan) · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The comprehensive screening of intracellular and extracellular microRNAs was performed to identify novel tumor suppressors. We found that miR-8073 was present in exosome and predominantly exported from colorectal cancer cells. Treatment with a synthetic miR-8073 mimic resulted in a dramatic decrease in the proliferation of various types of cancer cells, which was not observed in similarly treated normal cells. As little is known about the biological functions of miR-8073, its target mRNAs were analyzed by both mRNA expression and in silico sequence analyses, leading to five probable target candidates (FOXM1, MBD3, CCND1, KLK10, and CASP2) that enhance survival during the regulation of the cell cycle, cell proliferation, and apoptosis. We experimentally confirmed that miR-8073 binds the 3'-UTR of each of these mRNA target candidates and that the introduction of a synthetic miR-8073 mimic into cancer cells reduced levels of protein expression. Finally, the antiproliferative effects of miR-8073 were validated in vivo: the subcutaneous injection of a synthetic miR-8073 mimic suppressed colorectal tumor volume to 43% in tumor-bearing xenografted mice. These results suggest that because miR-8073 binds, and thus reduces the levels of, these oncogenic targets, cancer cells must actively downregulate miR-8073 as a survival mechanism. The introduction of miR-8073 into tumors could thus inhibit tumor growth, indicating its great potential for cancer therapeutics.

Indexed as

3' Untranslated RegionsA549 CellsAnimalsApoptosisCaspase 2Cell CycleCell Line, TumorCell ProliferationColorectal NeoplasmsCyclin D1Cysteine EndopeptidasesDNA-Binding ProteinsFemaleForkhead Box Protein M1Gene Expression Regulation, NeoplasticHCT116 Cells3' Untranslated RegionsCASP2 protein, humanCaspase 2CCND1 protein, humanCyclin D1Cysteine EndopeptidasesDNA-Binding ProteinsForkhead Box Protein M1FOXM1 protein, humanKallikreinsKLK10 protein, humanMBD3 protein, humanMicroRNAsRNA, Messenger

Identifiers

PMID30589909
PMCPMC6307750
OpenAlexW2908008901

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.