Evidence map›Paper›PMID 29925904›Full record

ArticleLeukemia2018

Inhibition of microRNA-138 enhances bone formation in multiple myeloma bone marrow niche.

Shokichi Tsukamoto, Marianne B Løvendorf, Jihye Park, Karma Z Salem, Michaela R Reagan, Salomon Manier, Oksana Zavidij, Mahshid Rahmat, Daisy Huynh, Satoshi Takagi and 10 more

Abstract read
PubMed Publisher
In one paragraph

Article in Leukemia, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

23 citing papers in PubMed, 41 citations in OpenAlex.

  1. Review
  2. MiR-376a-3p inhibits bone repair by regulating osteoblastic differentiation.Journal of orthopaedic surgery and research · 2025
    Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. MiR-138-5p Targets MACF1 to Aggravate Aging-related Bone Loss.International journal of biological sciences · 2022
    Article
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  12. Review
  13. Article
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  20. Observational
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

20 authors at 3 institutions in 3 countries.

Shokichi TsukamotoMedical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA, USA.
Marianne B LøvendorfMedical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA, USA.
Jihye ParkMedical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA, USA.
Karma Z SalemMedical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA, USA.
Michaela R ReaganMedical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA, USA.ORCID http://orcid.org/0000-0003-2884-6481
Salomon ManierMedical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA, USA.
Oksana ZavidijMedical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA, USA.
Mahshid RahmatMedical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA, USA.
Daisy HuynhMedical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA, USA.
Satoshi TakagiMedical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA, USA.
Yawara KawanoMedical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA, USA.ORCID http://orcid.org/0000-0002-8269-440X
Katsutoshi KokubunMedical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA, USA.
Charlotte Albæk ThrueCenter for RNA Medicine, Department of Clinical Medicine, Aalborg University Campus Copenhagen, Copenhagen, Denmark.ORCID http://orcid.org/0000-0003-1219-3447
Kenichi NaganoDepartment of Oral Medicine, Infection and Immunity, Harvard School of Dental Medicine, Harvard Medical School, Boston, MA, USA.ORCID http://orcid.org/0000-0003-3145-4841
Andreas PetriCenter for RNA Medicine, Department of Clinical Medicine, Aalborg University Campus Copenhagen, Copenhagen, Denmark.
Aldo M RoccaroMedical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA, USA.
Marzia CapellettiMedical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA, USA.
Roland BaronDepartment of Oral Medicine, Infection and Immunity, Harvard School of Dental Medicine, Harvard Medical School, Boston, MA, USA.
Sakari KauppinenCenter for RNA Medicine, Department of Clinical Medicine, Aalborg University Campus Copenhagen, Copenhagen, Denmark. ska@dcm.aau.dk.
Irene M GhobrialMedical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA, USA. irene_ghobrial@dfci.harvard.edu.
Harvard University · USAalborg University Hospital · DKMaine Medical Center · US

Funding

(PQ1) Genomic characterization of mesenchymal stromal cells in Monoclonal Gammopathy of Undermined Significance (MGUS)R01CA205954 · NCI · DANA-FARBER CANCER INST · PI GHOBRIAL, IRENE M. · 2016 to 2020
$2.6M
Stroma-mediated clonal evolution in Multiple MyelomaR01CA181683 · NCI · DANA-FARBER CANCER INST · PI GHOBRIAL, IRENE M. · 2014 to 2018
$1.8M
NCI NIH HHS R01 CA181683NCI NIH HHS R01 CA205954
6 · The paper itself

Abstract

Myeloma bone disease is a devastating complication of multiple myeloma (MM) and is caused by dysregulation of bone remodeling processes in the bone marrow microenvironment. Previous studies showed that microRNA-138 (miR-138) is a negative regulator of osteogenic differentiation of mesenchymal stromal cells (MSCs) and that inhibiting its function enhances bone formation in vitro. In this study, we explored the role of miR-138 in myeloma bone disease and evaluated the potential of systemically delivered locked nucleic acid (LNA)-modified anti-miR-138 oligonucleotides in suppressing myeloma bone disease. We showed that expression of miR-138 was significantly increased in MSCs from MM patients (MM-MSCs) and myeloma cells compared to those from healthy subjects. Furthermore, inhibition of miR-138 resulted in enhanced osteogenic differentiation of MM-MSCs in vitro and increased the number of endosteal osteoblastic lineage cells (OBCs) and bone formation rate in mouse models of myeloma bone disease. RNA sequencing of the OBCs identified TRPS1 and SULF2 as potential miR-138 targets that were de-repressed in anti-miR-138-treated mice. In summary, these data indicate that inhibition of miR-138 enhances bone formation in MM and that pharmacological inhibition of miR-138 could represent a new therapeutic strategy for treatment of myeloma bone disease.

Indexed as

OsteogenesisAnimalsBiomarkers, TumorBone MarrowCase-Control StudiesCell DifferentiationCells, CulturedFemaleFollow-Up StudiesGene Expression Regulation, NeoplasticHumansMaleMesenchymal Stem CellsMiceMice, Inbred C57BLMice, SCIDBiomarkers, TumorMicroRNAsMIRN138 microRNA, human

Identifiers

PMID29925904
OpenAlexW2808742475

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.