Turning off FSP1 forces lung cancer cells to collapse under their own stress, sharply reducing tumor growth.
Researchers at NYU Langone Health have discovered that a specific form of cell death triggered by the buildup of highly reactive molecules can help slow the growth of lung tumors.
This form of cell death, called ferroptosis, originally developed as a natural way for the body to remove cells experiencing extreme stress. Cancer cells also undergo this stress, yet they have adapted over time by developing defenses that prevent ferroptosis, allowing them to continue multiplying even when they are damaged.
A study published online November 5 in Nature reported that an experimental approach capable of blocking a protein known as ferroptosis suppressor protein 1 (FSP1) significantly reduced tumor growth in mice with lung adenocarcinoma (LUAD). Preventing FSP1 from functioning in cancer cells reduced tumor size by up to 80%. Lung cancer remains the leading cause of cancer-related deaths worldwide, and LUAD is the most common type among nonsmokers, accounting for about 40% of all cases.
“This first test of a drug that blocks ferroptosis suppression highlights the importance of the process to cancer cell survival and paves the way for a new treatment strategy,” said senior study author Thales Papagiannakopoulos, PhD, an associate professor in the Department of Pathology at the NYU Grossman School of Medicine.
