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miR-21 promotes the fibrotic properties in oral mucosa through targeting PDCD4
Yi-Wen Liao1, Lo-Lin Tsai2,3, Yu-Hsien Lee4,5
1Department of Medical Research, Chung Shan Medical University Hospital, Taichung, Taiwan.
Background/Purpose:
Oral submucous fibrosis (OSF) has been regarded as a premalignant disorder of oral cancer, and myofibroblasts are the main cells that are responsible for pathological fibrosis. Hence, elucidation of the molecular mechanism underlying myofibroblast activation is important to treat OSF. MicroRNA-21 (miR-21) is a well-known fibrosis non-coding RNA, and its role in the development of OSF remains largely unclear.
Materials And Methods:
Luciferase reporter assay was used to confirm the direct interaction between miR-21 and its target programmed cell death 4 (PDCD4). The expression level of PDCD4 in OSF was examined by qRT-PCR. Myofibroblast activities were assessed by collagen gel contraction and transwell migration assays.
Results:
Our result validated the direct binding of miR-21 to PDCD4. We showed the expression of PDCD4 was downregulated in OSF specimens and negatively correlated with miR-21. Our results suggested that overexpression of PDCD4 in fibrotic buccal mucosal fibroblasts (fBMFs) mitigated the myofibroblast activities, including collagen gel contractility and migration capacity. Moreover, we showed miR-21 contributed to myofibroblast activation of BMFs through repression of PDCD4.
Conclusion:
Our results suggest that the miR-21/PDCD4 axis mediates the myofibroblast activation of BMFs, and targeting this axis may exert an anti-fibrosis effect.
Insights
MicroRNA-21 (miR-21) activates myofibroblasts in oral submucous fibrosis (OSF) by downregulating PDCD4. Targeting the miR-21/PDCD4 pathway may offer a novel anti-fibrosis treatment for OSF.
Area of Science:
- Oral pathology
- Molecular biology
- Fibrosis research
Background:
- Oral submucous fibrosis (OSF) is a premalignant condition linked to oral cancer.
- Myofibroblasts drive pathological fibrosis in OSF.
- The role of microRNA-21 (miR-21) in OSF pathogenesis is not well understood.
Purpose of the Study:
- To investigate the molecular mechanism of myofibroblast activation in OSF.
- To elucidate the role of miR-21 and its target, programmed cell death 4 (PDCD4), in OSF development.
Main Methods:
- Luciferase reporter assay to confirm miR-21 and PDCD4 interaction.
- Quantitative reverse transcription PCR (qRT-PCR) to measure PDCD4 expression.
- Collagen gel contraction and transwell migration assays to assess myofibroblast activity.
Main Results:
- Direct binding of miR-21 to PDCD4 was validated.
- PDCD4 expression was downregulated in OSF tissues and inversely correlated with miR-21 levels.
- Overexpression of PDCD4 reduced myofibroblast activity (collagen gel contraction and migration).
- miR-21 promoted myofibroblast activation by repressing PDCD4.
Conclusions:
- The miR-21/PDCD4 axis is a key mediator of myofibroblast activation in OSF.
- Targeting this axis presents a potential therapeutic strategy for anti-fibrosis effects in OSF.
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