Abstract
Background Understanding the role of lncRNAs in the development of human malignancies is necessary for the targeted therapy of malignant tumors, including esophageal cancer (EC). Nevertheless, the specific role and regulatory mechanism of lncRNA WDFY3-AS2 in EC are still unclear. Here, we examined the functional role and regulatory mechanism of WDFY3-AS2 in EC. Materials and Methods RT-qPCR assay was applied to measure the expression of WDFY3-AS2 and miR-18a in EC samples and cells. The luciferase reporter and RIP assays were used to check the relationship between WDFY3-AS2, miR-18a, and PTEN. Counting Clock Kit-8 (CCK-8) assay was carried out to detect cell viability, and transwell assays were used for measuring cell migration and invasion. Results Underexpression of WDFY3-AS2 was found in EC specimens and cells, which predicted a poor prognosis of EC patients. Reexpression of WDFY3-AS2 repressed the progression of EC via inhibiting cell proliferation, migration, and invasion. Additionally, WDFY3-AS2 was negatively correlated with miR-18a and positively with PTEN. Furthermore, we discovered that the expression of PTEN decreased by miR-18a mimic was rescued by WDFY3-AS2 overexpression. Conclusions WDFY3-AS2 modulates the expressional level of PTEN as a competitive endogenous RNA via sponging miR-18a in EC, which suggests that the WDFY3-AS2/miR-18a/PTEN pathway might be involved in the progression of EC.
Highlights
Esophageal cancer (EC) is a malignant tumor with rapid progression and poor prognosis and is one of the most fatal diseases worldwide [1]
We hypothesized that WDFY3-AS2 plays a critical role in regulating esophageal cancer (EC) development with the implication of miR-18a and PTEN. us, we investigated the regulatory mechanism of WDFY3-AS2 in the regulation of EC cell proliferation, invasion, migration, and the relationships between WDFY3-AS2, miR-18a, and PTEN
36 EC patients were divided into a high expression group and a low expression group according to the average of WDFY3-AS2 expression
Summary
Esophageal cancer (EC) is a malignant tumor with rapid progression and poor prognosis and is one of the most fatal diseases worldwide [1]. Previous reports have discovered that LncRNAs play essential roles in the occurrence and development of EC [6]. There are enough pieces of evidence that dysregulation of lncRNAs that modulate cancer-related pathways could affect the progression of tumors, including EC [7]. Liang et al discovered that lnc01980 acted as an oncogenic lncRNA in modulating ESCC proliferation, migration, and invasion [9]. Understanding the role of lncRNAs in the development of human malignancies is necessary for the targeted therapy of malignant tumors, including esophageal cancer (EC). Reexpression of WDFY3-AS2 repressed the progression of EC via inhibiting cell proliferation, migration, and invasion. We discovered that the expression of PTEN decreased by miR-18a mimic was rescued by WDFY3-AS2 overexpression. WDFY3-AS2 modulates the expressional level of PTEN as a competitive endogenous RNA via sponging miR-18a in EC, which suggests that the WDFY3-AS2/miR-18a/PTEN pathway might be involved in the progression of EC
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