Regulation of protein import into Mitochondria in Colorectal cancer

Colorectal cancer (CRC) is the third leading cause of death in cancer patients in the US. Mitochondria are dynamic organelles that have essential metabolic activity, and their malfunction can thus influence CRC malignant transformation and tumour progression. Yet the mechanistic links between metastasis and mitochondrial dysfunction are only beginning to be elucidated. Recent studies reported that Tom34, a component of the mitochondrial protein import machinery, is over-expressed in CRC tissue. Cell proliferation is the driver  to initiate mitochondrial stress response due to increased demand for proteins. We thus hypothesize that mitochondrial protein import machinery is upregulated at the onset of CRC. Our lab aims is to understand the molecular function of the mitochondria import machinary and its role in mitochondrial adaption during cancer progression.