MARCHS is a key regulatory factor in mitochondria . However , the expression and function of MARCHS in thyroid cancer ( TC ) are not yet clear . The research explores the role and the potential mechanism of MARCH5 in the tumorigenesis of TC .MARCH5 expression were measured by qRT - PCR and Western blot . CCK -8 kits were used to measure the cell viability . Cell scratch assay and Tanswell assay were used to measure cell migration and invasion respectively . The pyroptosis related proteins (NLRP3, caspase -1, GSDMD ) and mitochondrial autophagy related proteins (LC3- II ,p62, parkin , pinkl ) were detected . The mitochondrial ROS GSH , MDA , and SOD were detected using commercial kits . Finally , a TC mouse model was constructed to detect the mle of MARCH5 in tumor growth in vivo . The results displayed that the expression of MARCH5 was increased in TC patients and cells and was significantly correlated with prognosis . Functional studies have found that MARCH5 inhi bits oxi dative stress levels and mitochondrial autophagy in TPC - I cells . Further research has found that MARCH5 promotes the progression of thyroid cancer by degrading FUNDC1 and inhibiting the mitochondrial autophagy mediated pyroptosis path - way , regulating cell proliferation , migration , and invasion in TPC -1 cells . More impor - tantly , interference with MARCH5 inhibits tumor growth and further development of TC in vivo . In conclusion ,MARCH5 promotes the progression of thymid cancer by degrad - ing FUNDCI and inhibiting the mitochondrial autophagy mediated pyroptosis , regulating cell proliferation , migration , and invasion . This study provides new theoretical basis for the treatment and prevention of TC in clinical practice .