Analysis and functional relevance of the chaperone TRAP-1 interactome in the metabolic regulation and mitochondrial integrity of cancer cells.

The 90 kDa heat shock protein, Hsp90, functions as a cancer chaperone contributing to tumor proliferation. We have encountered the mitochondrial homolog of Hsp90, the TRAP-1, regulating mitochondrial dynamics, metabolism, and tumor metastasis. Although Hsp90 is associated with a broad network of proteins regulating various cellular processes, TRAP-1-mediated cellular networks are unclear.

The mitochondrial chaperone TRAP-1 regulates the glutamine metabolism in tumor cells.

Understanding cancer cell metabolism always provides information on hidden dimensions of tumor adaptations. Warburg's theory that cancer cells opt for aerobic glycolysis over the mitochondrial oxidative phosphorylation (OXPHOS) system is widely accepted. However, the hypothesis does not explain the mitochondrion's role in these cells.

Mitochondrial chaperone, TRAP1 modulates mitochondrial dynamics and promotes tumor metastasis.

Mitochondria play a central role in regulating cellular energy metabolism. However, the present understanding of mitochondria has changed from its unipotent functions to pluripotent and insists on understanding the role of mitochondria not only in regulating the life and death of cells, but in pathological conditions such as cancer. Unlike other cellular organelles, subtle alterations in mitochondrial organization may significantly influence the balance between metabolic networks and cellular behavior.

Development of Nanocarrier-Based Mitochondrial Chaperone, TRAP-1 Inhibitor to Combat Cancer Metabolism.

Among human diseases, cancer has been in the frontlines of drug discovery and development. Despite having several decades of research efforts, therapeutic targeting of cancer is still challenging, which is due to the ability of cancer cells to adapt to the tumor microenvironment, exhibiting resistance to therapeutic drugs, and facilitated altered cancer metabolism. The small molecule inhibitors aimed at targeting a selective pathway are becoming void since cancer cells can activate alternate mechanisms.