Silencing SOX2OT reduces viability and migration in lung cancer cells via lncRNA and protein regulation.

Abstract

Long non-coding RNAs (lncRNAs) play crucial role in tumor development and are being explored as potential therapeutic targets in lung cancer. Both SOX2OT and SOX2 are consistently overexpressed in lung cancer, suggesting that SOX2OT may play a significant role in its development. This study examines how knocking down SOX2OT affects the expression of specific lncRNAs (LINC00982, LINC00668, SNHG7), the gene P16, and key cell cycle-regulating proteins (HSP90AA1, EP300, YES1) in lung cancer cells. Silencing of SOX2OT in A549 and Calu-3 cells led to a marked reduction in its expression. This downregulation was accompanied by decreased levels of SNHG7 and LINC00668, while LINC00982 and P16 transcripts were strongly induced. At the protein level, EP300, HSP90AA1, and YES1 were substantially reduced, whereas P16 was notably elevated. Functionally, suppression of SOX2OT impaired cell viability and significantly limited migratory capacity. In parallel, apoptosis assays demonstrated a pronounced increase in apoptotic cell populations following SOX2OT knockdown. SOX2OT regulates specific lncRNAs and proteins involved in lung cancer survival and migration. Silencing SOX2OT significantly reduces viability, migration, and survival of lung cancer cells, suggesting its potential as a therapeutic target. Further in vivo validation and rescue experiments are needed to confirm these mechanisms.