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Updated: Jul 8, 2025
In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice
Published on: August 23, 2019
miR-30a-5p targets ITGA6 to inhibit oral squamous cell carcinoma progression
Guodong Zhang1, Haiqin Wang2, Gui Liu1
1Hunan Key Laboratory of Oral Health Research & Hunan 3D Printing Engineering Research Center of Oral Care, Xiangya Stomatological Hospital & Xiangya School of Stomatology, Central South University, Changsha 410008, PR China.
Objective:
Nowadays, many studies focus on the relationship between microRNAs (miRs) and the development of oral squamous cell carcinoma (OSCC). Here, we broaden the understanding of miR-30a-5p in OSCC.
Methods:
In silico analysis was implemented to screen differentially expressed genes in OSCC and the related upstream regulatory miR. OSCC SCC9 cells were manipulated with lentivirus-mediated miR-30a-5p mimic, oe-ITGA6 or sh-ITGA6 and LY294002 (the PI3K/AKT pathway inhibitor) for studying their roles in cell biological processes. Tumors were xenografted in nude mouse for in vivo mechanism verification.
Results:
In silico analysis results depicted that ITGA6 was highly expressed in OSCC, and that miR-30a-5p was the upstream regulatory miR of ITGA6. miR-30a-5p was downregulated and ITGA6 was highly expressed in OSCC tissues and cells. miR-30a-5p targeted and downregulated ITGA6. ITGA6 promoted epithelial-mesenchymal transition, migration and invasion in OSCC cells by activating PI3K/AKT pathway. miR-30a-5p could suppress the in vivo growth and metastasis of OSCC by inhibiting the ITGA6/PI3K/AKT axis.
Conclusion:
Taken together, miR-30a-5p prevents OSCC progression by inhibiting PI3K/AKT pathway through inhibition of ITGA6 expression.
Insights
MicroRNA-30a-5p (miR-30a-5p) inhibits oral squamous cell carcinoma (OSCC) progression. It targets integrin alpha-6 (ITGA6), suppressing the PI3K/AKT pathway and reducing tumor growth and metastasis.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- MicroRNAs (miRs) play a crucial role in oral squamous cell carcinoma (OSCC) pathogenesis.
- Understanding specific miRs, like miR-30a-5p, is vital for OSCC research.
Purpose of the Study:
- To investigate the role of miR-30a-5p in OSCC.
- To elucidate the regulatory relationship between miR-30a-5p and ITGA6 in OSCC.
Main Methods:
- In silico analysis to identify differentially expressed genes and regulatory miRs in OSCC.
- In vitro studies using OSCC cells with lentivirus-mediated manipulation of miR-30a-5p, ITGA6, and PI3K/AKT pathway inhibitor.
- In vivo xenograft mouse models to validate the mechanism of action.
Main Results:
- ITGA6 was found to be highly expressed in OSCC, with miR-30a-5p acting as its upstream regulator.
- miR-30a-5p was downregulated, while ITGA6 was upregulated in OSCC tissues and cells.
- ITGA6 promoted OSCC cell epithelial-mesenchymal transition, migration, and invasion via PI3K/AKT pathway activation.
- miR-30a-5p suppressed OSCC growth and metastasis by inhibiting the ITGA6/PI3K/AKT axis.
Conclusions:
- miR-30a-5p acts as a tumor suppressor in OSCC.
- The miR-30a-5p/ITGA6/PI3K/AKT signaling pathway is a potential therapeutic target for OSCC treatment.
