The role of TRAP-1 in Mitochondria Transfer Between Cancer Cells

Abstract

The intercellular exchange of mitochondria, a well-established phenomenon known as 'mitochondrial transfer', has emerged as a fascinating phenomenon with implications in various physiological and pathological conditions, including cancer. Understanding the mechanisms governing mitochondrial transfer within the intricate landscape of cancer biology can provide new insights into novel therapeutic interventions. This study investigates the role of TNF receptor-associated protein 1 (TRAP-1), a molecular chaperone localized within the mitochondria, in mediating mitochondrial transfer between cancer cells. Through a series of experiments, we investigated the multifaceted interplay between TRAP-1 expression levels and mitochondrial dynamics within the neuronal cancer cells. We used TRAP-1 overexpression and knockdown cells to probe the consequences of TRAP1 modulation on mitochondrial transfer. We report that cells with altered TRAP1 levels exhibit actin reorganization. With the help of inducing oxidative stress and co-culture experiments, we aimed to elucidate the potential involvement of tunnelling nanotubes (TNT) in facilitating mitochondria transfer between cancer cells. We extended to exploring alternative mechanisms of mitochondrial exchange, particularly through extracellular vesicles and exosomes. The mitochondrial gene expression analysis provided insights that cancer cells utilize multiple routes for mitochondria transfer between cells. Overall, our study deepens understanding of mitochondrial transfer between cancer cells.