Glioma is one of the leading causes of
tumor-related deaths worldwide, but its potential mechanism remains unclear. This study aimed to explore the
biological role and potential mechanism of
argininosuccinate synthase 1 (ASS1) in
glioma. The relative expression levels of ASS1 in
glioma specimens and cell lines were calculated by quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and Western blotting. The
biological functions of ASS1 were demonstrated using the
5-ethynyl-2'-deoxyuridine (EdU) assay, transwell assay, and in vivo experiments. In addition, methylated
RNA immunoprecipitation (MeRIP),
RNA immunoprecipitation (RIP), and
luciferase reporter assays were performed to explore the molecular mechanism of ASS1 in
glioma. ASS1 expression levels were found to be downregulated in
glioma specimens and cell lines. Functionally, we confirmed that ASS1 inhibited
glioma cell proliferation, migration, invasion, and growth both. Furthermore, we found that ASS1 was a target of N(6)-adenosine-methyltransferase-14 (METTL14)-mediated
N6-methyladenosine (m6A) modification. Overexpression of METTL14 markedly elevated ASS1
mRNA m6A modification and suppressed ASS1
mRNA expression. We also revealed that METTL14-mediated ASS1 mRNA degradation relied on the YTH
m6A RNA-binding protein 2 (YTHDF2)-dependent pathway. We confirmed that decreased ASS1 expression promoted the cell proliferation, migration, and invasion in
glioma, and that the METTL14/ASS1/YTHDF2 regulatory axis may be an effective therapeutic target for
glioma.