Abstract
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.
Highlights
Known as a common malignancy in the digestive system, pancreatic carcinoma is a deadly disease
The results showed that high CTBP1‐AS2 expression was associated with lymph node metastasis and advanced clinical stage of patients with pancre‐ atic carcinoma
The results showed that the effects of CTBP1‐AS2 knockdown on pancreatic carcinoma cell proliferation, migration, invasion and apoptosis could be partially counteracted by inhibiting miR‐141‐3p (Fig. 3H‐M and Fig. S1)
Summary
Known as a common malignancy in the digestive system, pancreatic carcinoma is a deadly disease. Great progress has been made in surgical resection, radiotherapy and chemotherapy [2,3], the five‐year overall survival rate for patients with pancreatic carcinoma is only 8.3% [4]. Novel functional molecules in cancer biology have been identified. Long non‐coding RNAs (lncRNAs) have been demonstrated to be crucial regu‐ lators in tumorigenesis and cancer progression. LncRNAs have important biological functions and they partic‐ ipate in regulating tumor cell growth, migration, invasion and other malignant biological behaviors [5]. A number of lncRNAs have been shown to serve a role in pancreatic carcinoma development as cancer‐promoting factors or tumor suppressors, such as DNAH17‐AS1 [6], CASC2 [7] and SNHG16 [8]. The roles and mechanisms of lncRNAs in pancreatic carcinoma remain to be elucidated
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