Objectives
The objective of this research is to clarify the role and activity of LARP1 in the progression of ATC  and investigate its potential underlying mechanisms.

Methods
KMH-5M, CAL-62 cells and clinical ATC/PTC tissue samples were chosen as a model to study the effect of LARP1 in the progression of ATC. We performed cell functional tests such as CCK8 proliferation tests, colony formation tests, cell migration/invasion experiments, apoptosis assays, cell cycle assays, ROS induction, Immunohistochemistry and histology to assess the effects of LARP1 knockdown on cell cycle,  growth, colonies, movement, invasion，apoptosis and the level of ROS.

Results
By analyzing patient samples and ATC cell lines quantitatively, we discovered a notable increase in LARP1 expression in ATC tissues, which is associated with unfavorable patient outcomes. In laboratory experiments, it was shown that LARP1 supports various cancer-causing activities, such as blocking cell death and encouraging cell cycle advancement, growth, formation of colonies, movement, and invasion. Using transcriptomic analysis following LARP1 knockdown, cross-referenced against the LARP1 interactome, we identify TXNL2 and PRDX2 as LARP1 mRNA targets and  is associated with oxidative stress. We demonstrate that, through an interaction with the 3' untranslated regions (3' UTRs) of TXNL2 and PRDX2, LARP1 stabilizes ROS with the net effect of resisting apoptosis. 

Conclusions
Our research results offer persuasive evidence that LARP1 plays a significant role in the malignant advancement of ATC by interacting with the 3' untranslated regions (3' UTRs) of TXNL2 and PRDX2, leading to the stabilization of ROS. These insights deepen our understanding of ATC pathophysiology and suggest new avenues for therapeutic intervention. LARP1 could potentially be used as a valuable indicator for predicting outcomes and as a focus for future treatment approaches in ATC.