Long non‑coding RNAs (lncRNAs) feature prominently in pancreatic carcinoma progression. The present study aimed to clarify the biological functions, clinical significance and underlying mechanism of lncRNA CTBP1 antisense RNA 2 (CTBP1‑AS2) in pancreatic carcinoma. Reverse transcription‑quantitative PCR was performed to assess the expression levels of CTBP1‑AS2, microRNA (miR)‑141‑3p and ubiquitin‑specific protease 22 (USP22) mRNA in pancreatic carcinoma tissues and cell lines. Western blotting was used to examine USP22 protein expression in pancreatic carcinoma cell lines. Loss‑of‑function experiments were used to analyze the regulatory effects of CTBP1‑AS2 on proliferation, apoptosis, migration and invasion of pancreatic carcinoma cells. Dual‑luciferase reporter assay was used to examine the binding relationship between CTBP1‑AS2 and miR‑141‑3p, as well as between miR‑141‑3p and USP22. It was demonstrated that CTBP1‑AS2 expression was markedly increased in pancreatic carcinoma tissues and cell lines. High CTBP1‑AS2 expression was associated with advanced clinical stage and lymph node metastasis of patients. Functional experiments confirmed that knocking down CTBP1‑AS2 significantly inhibited pancreatic carcinoma cell proliferation, migration and invasion, and promoted cell apoptosis. In terms of mechanism, it was found that CTBP1‑AS2 adsorbed miR‑141‑3p as a molecular sponge to upregulate the expression level of USP22. In conclusion, lncRNA CTBP1‑AS2 may be involved in pancreatic carcinoma progression by regulating miR‑141‑3p and USP22 expressions; in addition, CTBP1‑AS2 may be a diagnostic biomarker and treatment target for pancreatic carcinoma.
Keywords: long non‑coding RNA CTBP1 antisense RNA 2; long non‑coding RNAs; microRNA‑141‑3p; pancreatic carcinoma; ubiquitin‑specific protease 22.