Effects of antisense lncRNA PCBP1-AS1 on biological behaviors of vulvar squamous carcinoma cells by regulating TRAF5 and NF-κB expression

BACKGROUND: Given antisense long noncoding RNAs (lncRNAs) poly C binding protein-1 antisense RNA1 (PCBP1-AS1) was significantly co-expressed with tumor necrosis factor receptor associated factor 5 (TRAF5) mRNA in vulvar squamous cell carcinoma (VSCC). TRAF5 could mediate nuclear factor kappa B (NF-κB) activation and regulate biological behaviors of tumor cells. Herein, we determined whether PCBP1-AS1 could affect the tumor behaviors of VSCC by regulating TRAF5 and NF-κB expression. METHODS: The expression of PCBP1-AS1 and TRAF5 mRNA in VSCC tissues and cells was detected via quantitative real-time polymerase chain reaction, while the protein expression levels of TRAF5, p65, p-p65, c-Rel, and IκBα were examined by immunoblotting. After the overexpression of PCBP1-AS1 and RNA interference knockdown of TRAF5 in SW954 cells, NF-κB activation-nuclear translocation fluorescence, the CCK-8 assay, Annexin V-FITC & PI fluorescent staining, the wound healing assay, and the Transwell invasion assay were performed to evaluate the activity of NF-κB, cellular proliferation, apoptosis, migration, and invasion. RESULTS: PCBP1-AS1 and TRAF5 mRNA expression were downregulated in VSCC tissues and were correlated with patient clinicopathological characteristics. The protein expression of TRAF5, p65, p-p65, c-Rel, and IκBα protein in VSCC tissues was significantly decreased. We demonstrated that PCBP1-AS1 positively regulated the expression of TRAF5. PCBP1-AS1 overexpression or knockdown of TRAF5 regulated the activity of the NF-κB pathway. Increase of PCBP1-AS1 significantly inhibited proliferation and enhanced apoptosis via TRAF5-mediated regulation of the NF-κB signaling pathway. Additionally, PCBP1-AS1 can suppress migration and invasion in an NF-κB-independent manner. CONCLUSIONS: As a tumor suppressor gene, PCBP1-AS1 regulates the proliferation and apoptosis of VSCC via TRAF5-mediated expression of the NF-κB.