The Knockdown of Inhibits the Papillary Thyroid Cancer Development by Promoting Ferroptosis Upon Downregulation

Papillary thyroid cancer (PTC) is one of the most prevalent endocrine malignancies. Herein, we aimed to provide a new viewpoint for the PTC progression and explore a new target for the effective therapy for PTC. We found that E26 transformation specific (ETS) variant 4 (, an ETS family transcription factor) was upregulated in PTC tissues and cells. experiments exhibited that silencing suppressed PTC cell proliferation and cell cycle progression, while the overexpression of gained the opposite results. Dual-luciferase reporter assay highlighted that could upregulate the solute carrier family 7 member 11 (, a key role for cysteine uptake in ferroptosis) transcription by binding to its promoter region directly. Moreover, the viability inhibition of PTC cells induced by the knockdown of was at least partly through the promotion of ferroptosis upon the downregulation of . In experiment, the results showed that the downregulation of repressed the tumor development through the low expression of , and the overexpression obtained the contrary effects. Overall, the data suggested that the knockdown of suppressed the PTC progression by promoting ferroptosis upon downregulation.