Abstract
BackgroundPancreatic cancer, one of the most aggressive malignancies, ranks the fourth cause of cancer-related death worldwide. Aberrantly expressed long non-coding RNAs (lncRNAs) functioned as oncogenes or tumor suppressors in pancreatic cancer. This study aimed to determine the expression of lncRNA DLX6 antisense RNA 1 (DLX6-AS1) in pancreatic cancer tissues and to explore the DLX6-AS1-related pathway in pancreatic cancer.Materials and methodsThe gene expression levels were determined by quantitative real-time PCR, and protein expression levels were determined by western blot assay. CCK-8 assay, colony formation assay and Transwell migration and invasion assays were used to examine cell proliferation, migration and invasion. Luciferase reporter assay was used to confirm the binding between DLX6-AS1and its potential targets. In vivo study used the mouse xenograft model to test the anti-tumor effect of DLX6-AS1 knockdown.ResultsThe high expression of DLX6-AS1 was observed in pancreatic cancer tissues, and high expression of DLX6-AS1 was positively correlated with larger tumor size, advanced TNM stage and lymph node metastasis. Knockdown of DLX6-AS1 dramatically impaired cancer cell proliferation, migration and invasion. MiR-181b was the downstream target of DLX6-AS1. Knockdown of miR-181b reversed the suppression of cell viability, migration and invasion abilities caused by DLX6-AS1 knockdown. MiR-181b was found to target Zinc finger E-box-binding homeobox 2 and to modulate epithelial-mesenchymal transition. Furthermore, DLX6-AS1 knockdown inhibited tumor growth and tumor metastasis in vivo.ConclusionCollectively, our data suggested that DLX6-AS1 promotes cancer cell proliferation and invasion by attenuating the endogenous function of miR-181b in pancreatic cancer.
Highlights
Pancreatic cancer, one of the most aggressive malignancies, ranks the fourth cause of cancer-related death worldwide
The high expression of DLX6-AS1 was observed in pancreatic cancer tissues, and high expression of DLX6AS1 was positively correlated with larger tumor size, advanced TNM stage and lymph node metastasis
Knockdown of miR-181b reversed the suppression of cell viability, migration and invasion abili‐ ties caused by DLX6-AS1 knockdown
Summary
Pancreatic cancer, one of the most aggressive malignancies, ranks the fourth cause of cancer-related death worldwide. Expressed long non-coding RNAs (lncRNAs) functioned as oncogenes or tumor suppres‐ sors in pancreatic cancer. This study aimed to determine the expression of lncRNA DLX6 antisense RNA 1 (DLX6-AS1) in pancreatic cancer tissues and to explore the DLX6-AS1-related pathway in pancreatic cancer. Pancreatic cancer, one of the most aggressive malignancies, ranks the fourth cause of cancer-related death. Surgery is the effective treatment for pancreatic cancer, the 5-year survival rate of the patients with pancreatic cancer is lower than 10% [1]. Chemotherapy remains the primary treatment and the combination therapy including FOLFIRINOX, paclitaxel and gemcitabine is the firstline drug, but the outcome is not satisfactory [3, 4]. The mechanisms underlying pancreatic cancer should be further investigated
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