Long Noncoding RNA WDFY3-AS2 Represses the Progression of Esophageal Cancer through miR-18a/PTEN Axis

Qingling Kong; Guangcai Li; Gang Yin; Kun Li; Dongqing Zhang; Weihao Xu

doi:10.1155/2021/9951010

Long Noncoding RNA WDFY3-AS2 Represses the Progression of Esophageal Cancer through miR-18a/PTEN Axis

J Oncol. 2021 Jun 5:2021:9951010. doi: 10.1155/2021/9951010. eCollection 2021.

Authors

Qingling Kong¹, Guangcai Li², Gang Yin³, Kun Li⁴, Dongqing Zhang⁵, Weihao Xu⁶

Affiliations

¹ Hospital Infection Control Office, Rizhao People's Hospital, Rizhao 276800, China.
² China-Canada International Health Management Center, Rizhao Hospital of TCM, Rizhao 276800, China.
³ Department of Clinical Laboratory, Affiliated Qingdao Central Hospital, Qingdao University, Qingdao 266042, China.
⁴ Department of Anesthesia, Zhangqiu District People's Hospital, Jinan 250200, China.
⁵ Department of Public Health, Zhangqiu District People's Hospital, Jinan 250200, China.
⁶ Medical Laboratory Center, Yantai Yuhuangding Hospital, Yantai 264000, China.

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.