4.4 Article

The potential influence of long non-coding RNA PRKG1-AS1 on oral squamous cell carcinoma: A comprehensive study based on bioinformatics and in vitro validation

Journal

JOURNAL OF ORAL PATHOLOGY & MEDICINE
Volume 49, Issue 5, Pages 409-416

Publisher

WILEY
DOI: 10.1111/jop.12980

Keywords

epithelial-mesenchymal transition; growth; invasion; migration; oral squamous cell carcinoma; protein kinase cGMP-dependent type I-antisense RNA 1

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Background Oral squamous cell carcinoma (OSCC) is one of the most frequent malignancies in oral cancer. Herein, we aimed to investigate the influence of lncRNA protein kinase cGMP-dependent type I-Antisense RNA 1 (PRKG1-AS1) in OSCC progression. Methods Basing on the data acquired from TCGA database, the expression and prognostic value of PRKG1-AS1 in OSCC patients were assessed. The expression of PRKG1-AS1 in OSCC cells was determined by quantitative real-time polymerase chain reaction (qRT-PCR). Cell growth was evaluated by Cell Counting Kit-8 (CCK8) and colony-forming assays. Transwell assay was employed to test cell invasion and migration. The protein expression of epithelial-mesenchymal transition (EMT)-related markers was detected by Western blotting. Results The consequences displayed that PRKG1-AS1 was highly expressed in OSCC tissues and high expression of PRKG1-AS1 predicted poor outcomes. The expression of PRKG1-AS1 was higher in CAL27, SCC-9, and SCC-4 than that in normal human oral keratinocytes (NHOK). The results of biological experiments showed that deficiency of PRKG1-AS1 suppressed cell growth, invasion, and migration in CAL27 cells, and over-expression of PRKG1-AS1 accelerated cell growth, invasion, and migration in SCC-4 cells. Finally, silencing of PRKG1-AS1 obviously facilitated the protein expression levels of E-cadherin and reduced levels of N-cadherin, Vimentin, and Snail in CAL27 cells whereas over-expression of PRKG1-AS1 led to opposite results in SCC-4 cells. Conclusion These outcomes indicated that PRKG1-AS1 functioned as a facilitator in OSCC cell growth, migration, and invasion, which all might be achieved by regulating EMT.

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