Long non-coding RNA (lncRNA) PGM5P4-AS1 inhibits lung cancer progression by up-regulating leucine zipper tumor suppressor (LZTS3) through sponging microRNA miR-1275. Issue 1 (1st January 2021)

• Record Type: Journal Article
• Authors: Feng, Junpeng; Li, Jianhang; Qie, Peng; Li, Zhenhua; Xu, Yanzhao; Tian, Ziqiang
• Is Part Of: Bioengineered. Volume 12:Issue 1(2021)
• Page Start: 196
• Page End: 207
• Publication Date: 2021-01-01
• Subjects: Lung cancer -- long non-coding RNA PGM5P4-AS1 -- microRNA miR-1275/leucine zipper putative tumor suppressor 3 -- proliferation -- metastasis; Biomedical engineering -- Periodicals; Biotechnology -- Periodicals; Microbiology -- Periodicals; 660.6
• DOI: 10.1080/21655979.2020.1860492
• Languages: English
• ISSNs: 2165-5987

Abstract

ABSTRACT: It is necessary to explore new molecules for the improvement of precise diagnosis and antitumor therapies in lung cancer. LncRNAs (long non-coding RNAs) play an important role in the regulation of cancer cell malignant behavior and tumor development. In this work, we found that a newly discovered lncRNA, lncRNA PGM5P4-AS1, was lower expressed in lung cancer tissues than adjacent tissues. Then, the lncRNA PGM5P4-AS1 was overexpressed or knocked-down in different lung cancer cells, and its effects on the malignant phenotypes were measured by 3-(4, 5-Dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) assay, cell cycle assay, wound healing assay, and transwell assay. The results showed that the overexpression of PGM5P4-AS1 inhibited lung cancer cell proliferation, migration, and invasion activities, while these abilities were prominently promoted by the interference of PGM5P4-AS1. Further, the growth of lung cancer tumors in nude mice was also inhibited by PGM5P4-AS1 overexpression. In mechanism, PGM5P4-AS1 has the binding site of miR-1275 and could positively regulate the expression of LZTS3 via sponging miR-1275. In conclusion, PGM5P4-AS1 could be a potential precise diagnosis and therapeutic target biomarker of lung cancer. GRAPHICAL ABSTRACT: