Role of lncRNA FAM83H antisense RNA1 (FAM83H-AS1) in the progression of non-small cell lung cancer by regulating the miR-545-3p/heparan sulfate 6-O-sulfotransferase (HS6ST2) axis. Issue 3 (1st March 2022)

• Record Type: Journal Article
• Authors: Zhang, Yue; Yu, Yue; Cao, Xuchen; Chen, Peng
• Is Part Of: Bioengineered. Volume 13:Issue 3(2022)
• Page Start: 6476
• Page End: 6489
• Publication Date: 2022-03-01
• Subjects: Lung cancer -- NSCLC -- FAM83H-AS1 -- miR-545-3p -- HS6ST2; Biomedical engineering -- Periodicals; Biotechnology -- Periodicals; Microbiology -- Periodicals; 660.6
• DOI: 10.1080/21655979.2022.2031668
• Languages: English
• ISSNs: 2165-5987

Abstract

ABSTRACT: Long non-coding RNAs (lncRNAs) are crucial regulators of cancer pathogenesis and are potentially useful diagnostic and prognostic biomarker tools. FAM83H antisense RNA1 (FAM83H-AS1) has been reported to be a vital regulator of different cancers; however, little attention has been paid to its significance in lung cancer. Non-tumorigenic lung cell line BEAS-2B and adenocarcinoma lung cancer cell lines NCI-H1299 and HCC827 were used in the present study. In addition, RNA immunoprecipitation, Western blotting, quantitative reverse transcription-PCR (qRT-PCR), and luciferase reporter assays were used to dissect the role of FAM83H-AS1 in lung cancer progression. The results revealed that FAM83H-AS1 is highly expressed in lung cancer tissues, and its knockdown inhibits lung cancer cell invasion and proliferation reducing tumor growth in vivo . Besides, we found that FAM83H-AS1 targets miR-545-3p, and a negative correlation exists between their expression in lung cancer tissues. Simultaneously, miR-545-3p negatively regulates heparan sulfate 6-O-sulfotransferase (HS6ST2). Moreover, inhibition of miR-545-3p promoted HS6ST2 protein expression and lung cancer cell invasion. FAM83H-AS1 favors non-small cell lung cancer by targeting the miR-545-3p/HS6ST2 axis, supporting the possibility of developing FAM83H-AS1 as a target for NSCLC intervention. Graphical abstract: uf0001