ASMTL‐AS1 impedes the malignant progression of lung adenocarcinoma by regulating SAT1 to promote ferroptosis
Xiujie Sui, Na Hu, Ze Zhang, Yirong Wang, Pengbo Wang, Guanghong Xiu
Abstract
Lung adenocarcinoma (LUAD) is difficult to cureradically. Long non-coding RNAs (lncRNAs) in LUAD are a hotspot in molecular research, however, the role of lncRNA ASMTL-AS1 in LUAD is still unknown. Our study explores the role and mechanisms of ASMTL-AS1 in LUAD. Quantitative reverse transcription PCR or western blot was utilized to analyze the expression of RNAs or proteins. The influences of ASMTL-AS1 and SAT1 on LUAD cells were analyzed by functional assays. Biological instruments were applied to observe ferroptosis-related markers. In vivo assays were performed to uncover the impact of ASMTL-AS1 on LUAD. Moreover, mechanism assays were done to confirm the relationship among ASMTL-AS1, SAT1 and U2AF2. Results showed that ASMTL-AS1 was down-regulated in LUAD cells and ASMTL-AS1 up-regulation resulted in retarded LUAD cell and xenograft tumor growth along with stimulated ferroptosis. ASMTL-AS1 recruited U2AF2 to stabilize SAT1 mRNA. Furthermore, SAT1 exerted a cancer suppressor role in LUAD cells. In conclusion, we first demonstrated that ASMTL-AS1 positively regulated SAT1 to promote ferroptosis and could stabilize SAT1 mRNA via recruiting U2AF2, shedding a light on a novel molecular mechanism in LUAD progression.