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Updated: Jun 6, 2026

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Published on: August 23, 2019
MicroRNA-124 suppresses oral squamous cell carcinoma motility by targeting ITGB1
Stuart Hunt1, Adam V Jones, Emma E Hinsley
1School of Clinical Dentistry, University of Sheffield, Sheffield, UK.
Abstract:
Alterations in the levels of molecules which interact with the extracellular matrix, such as integrins, are associated with invasion of oral squamous cell carcinomas (OSCC). The molecular mechanisms underlying dysregulation of integrin expression in OSCC, however, remain unclear. Here, we show that microRNA-124, a small non-coding RNA down-regulated in OSCC, is able to downregulate expression of integrin beta-1 (ITGB1) by interacting with its 3' untranslated region. Over-expression of miR-124 attenuates endogenous ITGB1 expression and reduces the adherence and motility of OSCC cells, suggesting disruption of miR-124-mediated repression of ITGB1 may be a key factor in OSCC progression.
Insights
MicroRNA-124 (miR-124) down-regulation in oral squamous cell carcinoma (OSCC) allows integrin beta-1 (ITGB1) to increase, promoting cancer cell invasion. Restoring miR-124 levels may inhibit OSCC progression.
Area of Science:
- Molecular biology
- Oncology
- Biochemistry
Background:
- Integrins mediate cell-extracellular matrix interactions crucial for cancer cell invasion.
- Dysregulation of integrin expression is observed in oral squamous cell carcinoma (OSCC) but underlying mechanisms are unclear.
Purpose of the Study:
- To investigate the role of microRNA-124 (miR-124) in regulating integrin expression in OSCC.
- To elucidate the molecular mechanisms by which miR-124 affects OSCC cell behavior.
Main Methods:
- Analysis of miR-124 levels in OSCC tissues.
- Investigating the interaction between miR-124 and the 3' untranslated region of integrin beta-1 (ITGB1) mRNA.
- Over-expression of miR-124 in OSCC cell lines.
Main Results:
- miR-124 was found to be down-regulated in OSCC.
- miR-124 directly targets and down-regulates ITGB1 expression.
- Over-expression of miR-124 reduced OSCC cell adherence and motility.
Conclusions:
- Down-regulation of miR-124 contributes to increased ITGB1 expression in OSCC.
- The miR-124/ITGB1 axis plays a significant role in OSCC cell invasion and motility.
- Restoring miR-124 levels presents a potential therapeutic strategy for OSCC.
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