MiR-23a Functions as a Tumor Suppressor in Osteosarcoma
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Background Osteosarcoma is the most common primary bone malignancy in children and adolescents, and the pathogenesis of this cancer remains unclear. Therefore, the discovery of new biomarkers for the diagnosis, prognosis, and treatment of osteosarcoma remains an important but unmet clinical need. Method Quantitative real-time PCR was carried out to examine the expression of miR-23a. Methylation-specific PCR was performed to evaluate the DNA methylation status of the miR-23a promoter. Cell proliferation, migration, and invasion were examined by cell counting assays, wound healing assays, and cell invasion assays, respectively. Western blot analysis and luciferase reporter assays were performed to identify miR-23 target genes. Nude mice were used to investigate the function of miR-23a in vivo. Results The expression of miR-23a was decreased in osteosarcoma cells and tissues compared to normal controls. The promoter region of the miR-23a gene was hypermethylated in osteosarcoma cells, and demethylase treatment increased the expression of miR-23a. The ectopic expression of miR-23a led to retarded proliferation, migration, and invasion of osteosarcoma cells, whereas the depletion of miR-23a resulted in the opposite effects. MiR-23a suppressed the transcription of RUNX2 and CXCL12 by binding to the 3' UTRs of these mRNAs. The cellular function of miR-23a is RUNX2/CXCL12-dependent, and the overexpression of RUNX2 or CXCL12 rescued the impaired cell growth, migration, and invasion in…
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Expression of miR-23a is reduced in osteosarcoma cells and tissues due to hypermethylation of its promoter region.
“the expression of miR-23a is reduced in osteosarcoma cells and tissues due to hypermethylation of its promoter region.”
From Recent advances of miR-23 in human diseases and growth development (2025) · cites this paper as [102]
Demethylation treatment can restore miR-23a expression.
“demethylation treatment can restore miR-23a expression.”
From Recent advances of miR-23 in human diseases and growth development (2025) · cites this paper as [102]
Ectopic expression of miR-23a significantly inhibits proliferation, migration, and invasion of osteosarcoma cells by targeting RUNX2 and CXCL12.
“Ectopic expression of miR-23a significantly inhibits the proliferation, migration, and invasion of osteosarcoma cells by targeting RUNX2 and CXCL12 in osteosarcoma”
From Recent advances of miR-23 in human diseases and growth development (2025) · cites this paper as [102]
Overexpression of miR-23 can significantly inhibit uPA expression and repress the invasive ability of multiple myeloma cells under in vitro and in vivo conditions.
“overexpression of miR-23 can significantly inhibit the uPA expression and then repress the invasive ability of multiple myeloma cells under in vitro and in vivo conditions [102,103].”
From Recent advances of miR-23 in human diseases and growth development (2025) · cites this paper as [102]
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Wade, S. M., Trenkmann, M., McGarry, T., Canavan, M., Marzaioli, V., Wade, S. C., Veale, D. J., & Fearon, U. (2019) · Journal of Autoimmunity · doi:10.1016/j.jaut.2018.08.008 · Cited by 35 · see citing works
Recent advances of miR-23 in human diseases and growth development
Qian, X., Jiang, Y., Yang, Y., Zhang, Y., Xu, N., Xu, B., Pei, K., Yu, Z., & Wu, W. (2025) · Non-coding RNA Research · doi:10.1016/j.ncrna.2024.12.010 · Cited by 5 · see citing works
- Authors
- He, Y., Meng, C., Shao, Z., Wang, H., & Yang, S.
- Affiliations
- Wuhan Union Hospital (CN)
- Venue
- Cellular Physiology and Biochemistry
- Publisher
- S. Karger AG
- Published
- 2014
- Volume
- 34
- Issue
- 5
- Pages
- 1485-1496
- ISSN
- 1015-8987 (ISSN-L)
- 1421-9778
- OpenAlex
- W2062766638
- Cited by
- 76
- References
- 1
- Citations by year
- 2026: 2 · 2024: 3 · 2023: 1 · 2022: 5 · 2021: 6 · 2020: 5 · 2019: 7 · 2018: 11 · 2017: 11 · 2016: 14 · 2015: 11
- FWCI
- 3.84
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Cellular Physiology and Biochemistry (publishedVersion, cc-by-nc)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › MicroRNA in disease regulation
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Sarcoma Diagnosis and Treatment
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer-related molecular mechanisms research
- Keywords
- miR-23a, osteosarcoma, tumor suppressor microRNA, DNA methylation, promoter hypermethylation, Runx2, CXCL12, cell proliferation, cell migration and invasion, 3' UTR target genes, diagnostic biomarkers
- MeSH terms
- Animals, Bone Neoplasms, Cell Line, Humans, Male, Mice, Inbred BALB C, Mice, Nude, Promoter Regions, Genetic, RNA, Messenger, Osteosarcoma, Gene Expression Regulation, Neoplastic, Genes, Tumor Suppressor, DNA Methylation, 3' Untranslated Regions, Tumor Suppressor Proteins, MicroRNAs, Cell Line, Tumor, Cell Proliferation, Core Binding Factor Alpha 1 Subunit, Mice, Chemokine CXCL12
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