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MiR-3612 targeting THBS1 suppresses nasopharyngeal carcinoma progression by PI3K/AKT signaling pathway.
- Source :
-
Human & Experimental Toxicology . Jan-Dec2023, Vol. 42, p1-10. 10p. - Publication Year :
- 2023
-
Abstract
- Background: MicroRNA-3612 (miR-3612) is considered a tumor suppressor in different cancers. Nonetheless, its function in nasopharyngeal carcinoma (NPC) has yet to be uncovered. Methods: NPC cells and tissues were tested by means of reverse transcription quantitative polymerase chain reaction (RT-qPCR) analysis and western blotting to quantify the expressions of miR-3612 and Thrombospondin 1 (THBS1). Cell Counting Kit-8 (CCK-8) and scratch experiments were carried out to evaluate the migration and proliferation of NPC cells. NPC cell adhesion was also assessed. The predicted interaction of miR-3612 with THBS1 was verified by means of a luciferase reporter assay. In vivo experiments were also conducted to examine how miR-3612 overexpression affects in vivo tumorigenicity. Lastly, phosphatidylinositol 3-kinase (PI3K)/AKT signaling pathway status was assessed via western blotting. Results: MiR-3612 was downregulated in NPC cells and tissues, whereas THBS1 expression showed an opposite trend. The MiR-3612 mimic inhibited the NPC cell proliferation, adhesion, and migration and also inactivated the PI3K/AKT signaling pathway. Furthermore, miR-3612 mimic also hampered NPC tumorigenesis in vivo. MiR-3612 targeted THBS1 and downregulated THBS1 expression. THBS1 offset the miR-3612-overexpression-induced repression of the migration, adhesion, and proliferation of NPC cells via the activation of the PI3K/AKT pathway. Conclusion: MiR-3612 retarded NPC cell migration, adhesion, and proliferation by targeting THBS1 and inactivating the PI3K/AKT signaling pathway. This provides a novel therapeutic approach for NPC intervention. [ABSTRACT FROM AUTHOR]
- Subjects :
- *NASOPHARYNX cancer
*DISEASE progression
*WESTERN immunoblotting
*PHOSPHOTRANSFERASES
*MICRORNA
*CELLULAR signal transduction
*GENE expression
*CELL motility
*TUMOR suppressor genes
*CELL proliferation
*DESCRIPTIVE statistics
*RESEARCH funding
*CELL adhesion molecules
*CELL lines
*DATA analysis software
*POLYMERASE chain reaction
Subjects
Details
- Language :
- English
- ISSN :
- 09603271
- Volume :
- 42
- Database :
- Academic Search Index
- Journal :
- Human & Experimental Toxicology
- Publication Type :
- Academic Journal
- Accession number :
- 175197529
- Full Text :
- https://doi.org/10.1177/09603271221150248