, and increased FASN expression has been viewed as a metabolic feature of cancer cells. Thus, FASN is considered a potential target to block tumor growth.
In their new paper, Jiang and colleagues used lung cancer cells to show that FASN inhibition induces reductive carboxylation, which further increases redox capacity in metastatic cancer cells. In this setting, reductive carboxylation induces a net cytosol-to-mitochondria citrate flux in FASN-deficient cells. This was surprising because citrate flux across mitochondria—one way that cancer cells gain energy—has been previously known to only go in the mitochondria-to-cytosol direction.
Building on prior research, this study provides additional data to support Jiang and his team's belief that targeting the cytosol-to-mitochondria citrate flux process can be an effective therapy for treating cancer patients with metastasis. Since the role of FASN in metastasis is context dependent, the team plans to test whether a similar mechanism exists in other cancer types beyond lung cancer.