Knockdown of MIR205HG prevents cell proliferation, migration and invasion through autophagy and ferroptosis pathways in lung adenocarcinoma.

Background: The MIR205 host gene (MIR205HG) has been reported to play important roles in various cancers. However, its role in the occurrence and development of lung cancer remains to be clarified. This study aimed to analyze the function and molecular mechanisms of MIR205HG in lung adenocarcinoma (LUAD). Methods: The RNA sequencing (RNA-Seq) dataset was used to examine MIR205HG expression. Quantitative reverse transcription polymerase chain reaction (qRT-PCR) was used to analyze the expression of MIR205HG in LUAD tissues and adjacent tissues. It was also employed to examine the expression of MIR205HG in LUAD cell lines. Water-Soluble Tetrazolium 1 (WST-1), colony formation assay, transwell assay and flow cytometry assay were used to explore the function of MIR205HG in lung cancer cells. Immunofluorescence assay was applied to examine the formation of autophagosomes. Western blot assay was used to analyze the expression of autophagy-related proteins and ferroptosis-related protein. Results: MIR205HG was highly expressed in LUAD tissues compared to adjacent tissues. Knockdown of MIR205HG expression prevented cell growth, migration, and invasion, and promoted apoptosis in LUAD cells. Western blot results showed that autophagy-related proteins, AMPK, BECLIN-1, and LC3B, were increased, while p62, mTOR and the ferroptosis-related protein GPX4 were decreased after MIR205HG knockdown. Conclusions: Knockdown of MIR205HG inhibits the development of LUAD through autophagy and ferroptosis pathways, suggesting that MIR205HG may be a potential target in the diagnosis and therapeutic treatment of LUAD.