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Roles of the H19/microRNA-675 axis in the proliferation and epithelial-mesenchymal transition of human cutaneous squamous cell carcinoma cells

The long non-coding RNA (lncRNA) H19 and microRNA(miR)-675 were reported to serve an important role in the tumorigenesis and metastasis of numerous cancer types by promoting the epithelial-mesenchymal transition (EMT) process; however, the underlying mechanisms of action of H19 and miR-675 in cutane...

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Detalles Bibliográficos
Autores principales: Zhang, Wenqing, Zhou, Kaili, Zhang, Xue, Wu, Chenglong, Deng, Dan, Yao, Zhirong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7905556/
https://www.ncbi.nlm.nih.gov/pubmed/33649811
http://dx.doi.org/10.3892/or.2021.7990
Descripción
Sumario:The long non-coding RNA (lncRNA) H19 and microRNA(miR)-675 were reported to serve an important role in the tumorigenesis and metastasis of numerous cancer types by promoting the epithelial-mesenchymal transition (EMT) process; however, the underlying mechanisms of action of H19 and miR-675 in cutaneous squamous cell carcinoma (cSCC) remain unknown. The mRNA expression levels of H19 and miR-675 were analyzed using reverse transcription-quantitative PCR, and Cell Counting Kit-8, wound healing and Transwell assays were performed to analyze the cell proliferation, migration and invasion of cSCC cells, respectively. The levels of cell apoptosis were also determined using a TUNEL assay. Protein expression levels of p53 and marker proteins related to the EMT process were analyzed using western blotting. In addition, a dual luciferase reporter assay was performed to determine the interactions between H19, miR-675 and p53. The results of the present study revealed that the expression levels of H19 and miR-675 were upregulated in cSCC tissues and cSCC cell lines. The knockdown of H19 or miR-675 expression inhibited cell proliferation, migration and invasion, but induced cell apoptosis. In addition, the expression levels of EMT-related markers were also downregulated. The overexpression of H19 upregulated the expression levels of its predicted target, miR-675, which subsequently promoted the EMT process and downregulated the expression levels of p53. Conversely, the genetic silencing of H19 or miR-675 inhibited proliferation and invasion in SCL1 and A431 cSCC cell lines. In conclusion, the findings of the present study provided novel insight into the potential role of H19 and miR-675 in the development, metastasis and progression of cSCC, which may help the development of treatments for cSCC.