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Fabrication of Tongue Extracellular Matrix and Reconstitution of Tongue Squamous Cell Carcinoma In Vitro
Published on: June 20, 2018
miR-27b Suppresses Tongue Squamous Cell Carcinoma Epithelial-Mesenchymal Transition by Targeting ITGA5
Tao Li1, Qian Wu2, Duanqin Liu1
1Department of Oral and Maxillofacial Surgery, School and Hospital of Stomatology, Cheeloo College of Medicine, Shandong University & Shandong Key Laboratory of Oral Tissue Regeneration & Shandong Engineering Laboratory for Dental Materials and Oral Tissue Regeneration, Jinan, Shandong, People's Republic of China.
Background:
MicroRNA27b-3p (miR-27b) has been reported to be dysregulated in multiple types of human cancer. However, the expression levels, biological roles, and underlying mechanism of miR-27b in tongue squamous cell carcinoma (TSCC) remain to be elucidated.
Methods:
Bioinformatics analyses and quantitative real-time PCR (qRT-PCR) were used to determine miR-27b expression in TSCC tissues and cell lines. The influence of miR-27b overexpression or inhibition on TSCC cell proliferation, migration, and invasion in vitro, and on tumor growth in vivo, was explored via CCK8, colony formation, wound healing, and transwell assays, and in xenograft tumors in nude mice, respectively. Luciferase reporter assays, qRT-PCR, and Western blotting were performed to clarify the potential mechanisms involving miR-27b in TSCC cells.
Results:
miR-27b was significantly downregulated in TSCC tissues and cell lines, and its expression was correlated with cancer status. Overexpression of miR-27b led to diminished proliferation, migration, and invasion, and notably reduced tumor growth in vivo. Bioinformatics analysis followed by luciferase reporter assays demonstrated that miR-27b expression was inversely correlated with that of integrin subunit α5 (ITGA5)and that miR-27b directly bound to the 3'-untranslated region of ITGA5 in TSCC cells. The bioinformatics analysis also indicated that ITGA5 was upregulated in TSCC and that its expression was correlated with epithelial-mesenchymal transition (EMT) and poor prognosis. Moreover, we found that miRNA-27b could reverse ITGA5-induced promotion of TSCC cell proliferation and migration. Finally, we demonstrated that regulation of miR-27b expression in TSCC may result in alterations in the expression of ITGA5 and EMT-related marker genes at the mRNA and protein levels.
Conclusion:
These results indicate that miR-27b hampers TSCC proliferation and migration via suppressing the EMT process by targeting ITGA5. These findings support consideration of miR-27b/ITGA5 as a valuable marker for the metastatic potential of TSCC, or as a therapeutic target for the treatment of TSCC.
Insights
MicroRNA-27b (miR-27b) is downregulated in tongue squamous cell carcinoma (TSCC) and suppresses tumor growth by targeting integrin subunit α5 (ITGA5). Restoring miR-27b inhibits TSCC progression and EMT, suggesting a therapeutic target.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- MicroRNA27b-3p (miR-27b) dysregulation is noted in various cancers.
- The role of miR-27b in tongue squamous cell carcinoma (TSCC) is not fully understood.
Purpose of the Study:
- To investigate the expression, biological functions, and regulatory mechanisms of miR-27b in TSCC.
- To explore the potential of the miR-27b/ITGA5 axis as a therapeutic target for TSCC.
Main Methods:
- Quantitative real-time PCR (qRT-PCR) and bioinformatics analyses were used to assess miR-27b expression.
- In vitro and in vivo assays evaluated the effects of miR-27b on TSCC cell proliferation, migration, invasion, and tumor growth.
- Luciferase reporter assays, qRT-PCR, and Western blotting identified miR-27b's molecular targets and mechanisms.
Main Results:
- miR-27b was significantly downregulated in TSCC tissues and cell lines.
- miR-27b overexpression inhibited TSCC cell proliferation, migration, invasion, and tumor growth.
- miR-27b directly targets integrin subunit α5 (ITGA5), suppressing its expression and reversing ITGA5-induced TSCC progression and EMT.
Conclusions:
- miR-27b suppresses TSCC progression and epithelial-mesenchymal transition (EMT) by targeting ITGA5.
- The miR-27b/ITGA5 axis is a potential biomarker for TSCC metastatic potential and a therapeutic target.
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