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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
Author(s) -
Wu Ting,
Zhang ShiYang,
Dong WenJie,
Wang Mei,
Sun YuBin
Publication year - 2020
Publication title -
journal of oral pathology and medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.887
H-Index - 83
eISSN - 1600-0714
pISSN - 0904-2512
DOI - 10.1111/jop.12980
Subject(s) - vimentin , biology , cancer research , cell , cell growth , cell migration , gentamicin protection assay , gene silencing , antisense rna , long non coding rna , cell culture , blot , small interfering rna , in vitro , real time polymerase chain reaction , microbiology and biotechnology , rna , cancer , metastasis , immunology , transfection , immunohistochemistry , gene , biochemistry , genetics
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.