ICT1 has been recognized for its overexpression in several cancer types, such as hepatoblastoma, glioblastoma multiforme, and non-small cell lung cancer . In colorectal cancer (CRC), ICT1 expression correlates with unfavorable prognosis and reduced survival rates . Studies have shown that ICT1 promotes CRC growth through intracellular signaling pathways, including AMPK, SAPK/JNK, and PARP .
ICT1 functions as a component of the mitochondrial ribosome (mitoribosome) and exhibits peptidyl-tRNA hydrolase (PTH) activity via the tripeptide motif GGQ . This activity is crucial for maintaining mitochondrial protein synthesis and overall cellular function. Depletion of ICT1 disrupts mitoribosomal structure, leading to decreased mitochondrial membrane potential and mass .
Research has demonstrated that knockdown of ICT1 induces suppression of cell proliferation, S-phase arrest, and apoptosis in leukemia cells . This suggests that ICT1 could be a potential therapeutic target for treating various cancers. In CRC, ICT1 silencing has been shown to lower cell viability, inhibit cell migration, and induce apoptosis .