Evidence map›Paper›PMID 31284378›Full record

ArticleInternational journal of molecular sciences2019

CCN3 Facilitates Runx2 and Osterix Expression by Inhibiting miR-608 through PI3K/Akt Signaling in Osteoblasts.

Po-Chun Chen, Ju-Fang Liu, Yi-Chin Fong, Yuan-Lin Huang, Chia-Chia Chao, Chih-Hsin Tang

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
2.1field-weighted citation impact, top 12% 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

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

  1. Pooled it
  2. Review
  3. Article
  4. Review
  5. Article
  6. Role and mechanism of Integrin α5β1 in bone formation and disease.Frontiers in cell and developmental biology · 2025
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Myeloid CCN3 protects against aortic valve calcification.Cell communication and signaling : CCS · 2023
    Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. Article
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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

6 authors at 3 institutions in 1 country.

Po-Chun ChenCentral Laboratory, Shin-Kong Wu Ho-Su Memorial Hospital, Taipei 111, Taiwan.
Ju-Fang LiuCentral Laboratory, Shin-Kong Wu Ho-Su Memorial Hospital, Taipei 111, Taiwan.
Yi-Chin FongDepartment of Sports Medicine, College of Health Care, China Medical University, Taichung 404, Taiwan.
Yuan-Lin HuangDepartment of Biotechnology, College of Health Science, Asia University, Taichung 413, Taiwan.
Chia-Chia ChaoDepartment of Respiratory Therapy, Fu-Jen Catholic University, New Taipei City 242, Taiwan.
Chih-Hsin TangDepartment of Biotechnology, College of Health Science, Asia University, Taichung 413, Taiwan. chtang@mail.cmu.edu.tw.ORCID 0000-0002-7113-8352
Asia University · TWChina Medical University · TWFu Jen Catholic University · TW

Funding

China Medical University CMU 103-ASIA-03Taiwan's Ministry of Science and Technology MOST 107-2320-B-341-001-MY2
6 · The paper itself

Abstract

CCN3, otherwise known as the nephroblastoma overexpressed (NOV) protein, is a cysteine-rich protein that belongs to the CCN family and regulates several cellular functions. Osteoblasts are major bone-forming cells that undergo proliferation, mineralization, renewal, and repair during the bone formation process. We have previously reported that CCN3 increases bone morphogenetic protein 4 (BMP-4) production and bone mineralization in osteoblasts, although the role of CCN3 remains unclear with regard to osteogenic transcription factors (runt-related transcription factor 2 (Runx2) and osterix). Here, we used alizarin red-S and alkaline phosphatase staining to show that CCN3 enhances osteoblast differentiation. Stimulation of osteoblasts with CCN3 increases expression of osteogenic factors such as BMPs, Runx2, and osterix. Moreover, we found that the inhibition of miR-608 expression is involved in the effects of CCN3 and that incubation of osteoblasts with CCN3 promotes focal adhesion kinase (FAK) and Akt phosphorylation. Our results indicate that CCN3 promotes the expression of Runx2 and osterix in osteoblasts by inhibiting miR-608 expression via the FAK and Akt signaling pathways.

Indexed as

OsteogenesisSignal Transduction3' Untranslated RegionsAnimalsBase SequenceCell LineCore Binding Factor Alpha 1 SubunitFocal Adhesion Protein-Tyrosine KinasesHumansMicroRNAsNephroblastoma Overexpressed ProteinOsteoblastsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSp7 Transcription Factor3' Untranslated RegionsCCN3 protein, humanCore Binding Factor Alpha 1 SubunitFocal Adhesion Protein-Tyrosine KinasesMicroRNAsMIRN608 microRNA, humanNephroblastoma Overexpressed ProteinPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSp7 Transcription FactorCCN3miR-608osteoblastsosterixRunx2

Identifiers

PMID31284378
PMCPMC6651805
OpenAlexW2955372952

What OpenQuestion holds

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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.