Lipid peroxidation in cancer: a double-edged sword shaping progression and therapy

Lipid Peroxidation (LPO) is a process driven by oxidative stress that is notoriously implicated for triggering various diseases. In cancer, however, LPO acts as a double-edged sword, fueling tumor growth while showing promise as a treatment target. This review performs a deep dive into this duality and highlights its twofold involvement across various malignancies, including colorectal, breast, and lung cancers. LPO is closely linked with oxidative stress, which contributes to DNA damage, chronic inflammation, and other processes that cause cancer initiation. Other LPO-derived mechanisms, such as the production of destructive reactive aldehydes, NF-κB activation, and immune evasion, are also examined, showing LPO's ability to fuel tumor growth and expansion. In contrast, LPO's destructive power can be redirected to target cancer cells by inhibiting key antioxidant enzymes or silencing Nrf2. Although further research is critically needed to refine these approaches, they represent promising new avenues for treating cancers that resist conventional therapies and may help guide future precision oncology strategies.