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CircSERPINA3 promoted cell proliferation, migration, and invasion of laryngeal squamous cell carcinoma by targeting miR‐885‐5p.
- Source :
-
Cell Biology International . Nov2022, Vol. 46 Issue 11, p1852-1863. 12p. - Publication Year :
- 2022
-
Abstract
- CircSERPINA3 has been shown to be upregulated in laryngeal squamous cell carcinoma (LSCC); however, whether it regulates the development of LSCC and the specific molecular mechanism remains unclear, which is to be explored in this study. Expressions of circSERPINA3, miR‐885‐5p, and Malic enzyme 1 (ME1) in LSCC tissues or cell lines were determined by quantitative reverse transcription polymerase chain reaction (qRT‐PCR). The regulation of circSERPINA3 on the biological behavior of LSCC cells was confirmed by loss and gain experiments (cell counting kit‐8, transwell, and colony formation assay). The correlation between circSERPINA3/ME1 and miR‐885‐5p was predicted and confirmed by bioinformatics analysis, dual‐luciferase reporter assay, and qRT‐PCR. The effect of circSERPINA3/miR‐885‐5p axis on the biological behavior of LSCC cells and expressions of epithelial–mesenchymal transition‐related proteins was confirmed by rescue experiments. CircSERPINA3 and ME1 was upregulated in LSCC tissues, whereas miR‐885‐5p was downregulated. MiR‐885‐5p was the target gene of circSERPINA3, whereas ME1 was the target gene of miR‐885‐5p. Silent circSERPINA3 suppressed viability, invasion, migration, colony formation, and expression of ME1, claudin‐4, snail, and vimentin but elevated expression of miR‐885‐5p and E‐cadherin, whereas overexpressed circSERPINA3 was the opposite. However, miR‐885‐5p inhibitor or mimic reversed the effects of silent circSERPINA3 or overexpressed circSERPINA3. Collectively, circSERPINA3 promotes proliferation, migration, and invasion of LSCC cells by targeting miR‐885‐5p. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 10656995
- Volume :
- 46
- Issue :
- 11
- Database :
- Academic Search Index
- Journal :
- Cell Biology International
- Publication Type :
- Academic Journal
- Accession number :
- 159611317
- Full Text :
- https://doi.org/10.1002/cbin.11872