The long noncoding RNA FAM83H-antisense RNA 1 (FAM83H-AS1) is involved in gastric cancer (GC) development. This study determined whether FAM83H-AS1 was regulated by N6-methyladenosine (m6A) modifications in GC. Real-time quantitative polymerase chain reaction was performed to determine the expression levels of FAM83H-AS1 and Wilms' tumor 1 associated protein (WTAP). The protein content of WTAP was evaluated using western blotting. To assess the m6A alterations in FAM83H-AS1, methylated RNA immunoprecipitation was performed to identify interactions between WTAP and FAM83H-AS1. Functionally, the proliferation, migration, and invasion of GC cells were measured using a Cell Counting Kit-8 and transwell assays, respectively. High expression levels of FAM83H-AS1 and WTAP were detected in GC samples and there was a positive correlation between them. In addition, WTAP mediates FAM83H-AS1 expression in an m6A-dependent manner. Further investigations indicated that WTAP silencing reversed the cancer-promoting role of FAM83H-AS1 overexpression in GC cell migration, proliferation, and invasion. Our results suggest that WTAP-mediated FAM83H-AS1 promotes GC development via m6A modification. Our findings provide new biomarkers for GC diagnosis and targeted therapy. Wilms' tumor 1 associated protein (WTAP) promotes gastric cancer (GC) by accelerating cell proliferation, migration, and invasion of GC cells via the N6-methyladenosine(m6A) modification of long non coding RNA FAM83H-AS1.
Keywords: FAM83H-AS1; Gastric cancer; Wilms’ tumor 1 associated protein; m6A modification.
© 2023. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.