Immt, also known as inner membrane mitochondrial protein, encodes MIC60 which is a key component of the mitochondrial contact site and cristae organizing system (MICOS). MICOS is crucial for crista junction formation and maintaining inner mitochondrial membrane architecture [2]. Immt is involved in processes like mitophagy, which is essential for mitochondrial quality control, and has significance in maintaining cellular homeostasis [1].

Genetic ablation of Immt in adult mice via tamoxifen-inducible ROSA-CreERT2-mediated deletion disrupts the MICOS complex, increases mitochondria size, alters cristae morphology, and leads to lethal outcomes within 12 days. Pathologically, these mice show defective intestinal muscle function (paralytic ileus) and bone marrow hypocellularity [2].

In lung adenocarcinoma, high-IMMT expression is related to advanced disease stage, larger tumor size, intratumoral vascular invasion, and poorer patient prognosis. Knockdown of IMMT in A549 cells decreases cell proliferation [3].

In breast cancer, high IMMT expression serves as an independent diagnostic biomarker, correlates with advanced clinical status, and indicates a poor relapse-free survival rate. Experimental knockdown of IMMT impedes cell migration and viability, arrests the cell cycle, disturbs mitochondrial function, and increases ROS level and lipid peroxidation [4].

In conclusion, Immt is vital for maintaining mitochondrial structure and function, especially through its role in the MICOS complex. Studies using Immt-deleted mouse models have revealed its significance in lethal disruptions of mitochondrial function and in disease conditions such as lung and breast cancers, highlighting its potential as a prognostic indicator and therapeutic target in these cancer types.