Scientists from the VIB–KU Leuven Center for Cancer Biology and the Francis Crick Institute announced on Mar. 17 that they have identified a way cancer cells exploit healthy lung cells to support metastatic tumor growth in the lungs. The findings, published in Nature Cell Biology and Cancer Discovery, show that tumors use lipids produced by lung cells as signals, and that decreasing this lipid production can reduce metastasis.
Metastasis is a major reason why cancer remains one of the leading causes of death worldwide. The lungs are a common site for secondary tumors, especially in breast cancer cases. Once metastases form, treatment options become limited and prognosis worsens.
The research focused on alveolar type II (AT2) cells—lung-resident cells previously shown to prepare organs for incoming cancer cells. According to Dr. Xiao-Zheng Liu, "We discovered that cancer cells recruit AT2 cells and reprogram them to produce more lipids for them." Liu also said, "Rather than targeting cancer cells directly, it may also be possible to target other cells that boost their growth, which could open new options for possible treatments."
The collaboration between institutes strengthened the results. Prof. Mariia Yuneva said, "We were able to obtain the same results in different laboratories, with different models and with different techniques. Bringing our complementary expertise together made the study very robust." Further investigation revealed that lipids supplied by AT2 cells serve not only as an energy source but also act as signals modifying proteins within cancer cells. Dr. Ming Liu explained, "By studying a specific lipid component called palmitate, we identified the pathway that triggers these molecular changes in the cell and promotes lung metastasis." Prof. Sarah-Maria Fendt added, "The key insight was that these lipids are not just used as an energy source. Instead, they initiate the molecular pathway that enables cancer cells to modify themselves and grow. When we interrupt this process, we can block metastatic growth."
Several clinical trials are currently investigating drugs that inhibit lipid production; however, identifying patients who will benefit most remains challenging. Prof. Fendt said, "Our findings suggest that these inhibitors may best work in patients whose metastasis recruit large amounts of AT2 cells. This insight helps refine the group of patients who may benefit most from these therapies." The studies also suggest AT2 cell lipid metabolism could play a role in primary lung cancers.
