PRKCZ-AS1 promotes the tumorigenesis of lung adenocarcinoma via sponging miR-766-5p to modulate MAPK1. Issue 4 (2nd April 2020)

• Record Type: Journal Article
• Authors: Wang, Ming; Liao, Qin; Zou, Pengfei
• Is Part Of: Cancer biology & therapy. Volume 21:Issue 4(2020)
• Page Start: 364
• Page End: 371
• Publication Date: 2020-04-02
• Subjects: LUAD -- PRKCZ-AS1 -- miR-766-5p -- MAPK1; 616.99406
• DOI: 10.1080/15384047.2019.1702402
• Languages: English
• ISSNs: 1538-4047

Abstract

ABSTRACT: Lung adenocarcinoma (LUAD) is the most prevalent histological subclass of non-small cell lung cancer. Long non-coding RNAs (lncRNAs) have been recognized as the crucial regulatory factors in tumor development and progression. Nevertheless, limited research has been carried on the function of PRKCZ-AS1 in LUAD. In this study, the expression of PRKCZ-AS1 in LUAD tissues and cell lines was notably upregulated. Moreover, knockdown of PRKCZ-AS1 inhibited the proliferation and migration, but promoted apoptosis in LUAD cells. Furthermore, miR-766-5p could bind with PRKCZ-AS1. Besides, the expression miR-766-5p was negatively regulated by PRKCZ-AS1 expression in LUAD cells. Furtherly, PRKCZ-AS1 expression positively regulated the expression of MAPK1. Similarly, the expression of MAPK1 was negatively regulated by miR-766-5p expression. Moreover, the binding ability between miR-766-5p and MAPK1 was confirmed. Furthermore, knockdown of MAPK1 partly rescued the miR-766-5p inhibition-mediated promoting effect on proliferation and migration in LUAD cells transfected with PRKCZ-AS1#1. Overall, above results suggested that PRKCZ-AS1 promotes the occurrence of LUAD by sponging miR-766-5p to upregulate MAPK1 expression, which may provide new insights into LUAD treatment.