Dihydroartemisinin inhibits IL-6-induced epithelial–mesenchymal transition in laryngeal squamous cell carcinoma via the miR-130b-3p/STAT3/β-catenin signaling pathway
Objective To explore whether dihydroartemisinin (DHA) can block interleukin (IL)-6-induced epithelial–mesenchymal transition (EMT) in laryngeal squamous cell carcinoma (LSCC). Methods The expression of SLUG, signal transducer and activator of transcription 3 (STAT3), and microRNA (miR)-130b-3p was m...
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| Autores principales: | , , , |
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| Formato: | article |
| Lenguaje: | EN |
| Publicado: |
SAGE Publishing
2021
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| Materias: | |
| Acceso en línea: | https://doaj.org/article/cb8a7bb368aa41fc9077f98c5913a329 |
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| Sumario: | Objective To explore whether dihydroartemisinin (DHA) can block interleukin (IL)-6-induced epithelial–mesenchymal transition (EMT) in laryngeal squamous cell carcinoma (LSCC). Methods The expression of SLUG, signal transducer and activator of transcription 3 (STAT3), and microRNA (miR)-130b-3p was measured. In addition, a dual-luciferase reporter assay was performed to examine the interaction of miR-130b-3p with STAT3. Results We found that IL-6 can promote EMT and invasion in LSCC cells, whereas DHA can inhibit these two processes. However, DHA alone does not influence EMT and cancer invasion. Furthermore, DHA upregulated miR-130b-3p, which can downregulate STAT3 and β-catenin protein expression and decrease the activity of the IL-6/STAT3 signaling pathway. Moreover, we found that miR-130b-3p can target STAT3 directly. Conclusions DHA can block IL-6-triggered EMT and invasion in LSCC, and during these processes, DHA increases miR-130b-3p expression to decrease the activation of the IL-6/STAT3 and β-catenin signaling pathways. These findings may provide new insights into strategies for suppressing and even preventing LSCC metastasis. |
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