PRKCZ-AS1 promotes the tumorigenesis of lung adenocarcinoma via sponging miR-766-5p to modulate MAPK1

PRKCZ-AS1通过海绵吸附miR-766-5p来调节MAPK1,从而促进肺腺癌的肿瘤发生。

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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.

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