Korean Scientists Uncover Key to Battling Drug-Resistant Breast Cancer by Targeting Fat Cells

Korean researchers have unveiled a groundbreaking strategy to combat drug-resistant breast cancer, not by solely attacking cancer cells, but by disarming their fatty enablers. A joint team led by Professor Sun-Young Kong and Professor Byung-Heon Kang discovered that a mitochondrial protein called TRAP1 plays a crucial role in transforming normal fat cells into 'cancer-associated adipocytes' (CAAs) that actively fuel tumor growth and resistance to treatments. Suppressing TRAP1 in these fat cells significantly shrunk tumors by up to 56% in mouse models, and when combined with existing chemotherapy, led to a remarkable 76% reduction. This breakthrough addresses a critical challenge in oncology: how breast cancer often develops resistance to current drug regimens, a problem frequently amplified by the tumor's surrounding environment. These CAAs, found abundantly around breast tumors, secrete inflammatory substances and supply vital nutrients, effectively creating a sanctuary for cancer cells to thrive and evade treatment. The research highlights a shift towards understanding and targeting the tumor microenvironment, offering a fresh angle beyond directly targeting cancer cells, which often adapt and develop resistance. The findings have already moved to the next stage, with SmartinBio, a faculty startup from UNIST, actively developing an oral TRAP1 inhibitor for clinical use, demonstrating its promise for patients who don't respond well to current anticancer drugs. Researchers are optimistic this strategy could also be effective against other cancers that develop near fatty tissues, such as ovarian, pancreatic, and prostate cancers. The team plans further studies to assess its application in clinical settings, opening a new avenue for next-generation cancer therapies.