How 'undead' cells trigger cancer-promoting inflammation
Stopping tumor growth is only half the battle. Rather than killing tumor cells, many cancer therapies can only push them into cellular senescence, a state in which cells stop dividing but do not die. These "undead" cells continue to release signals that reshape the tumor environment. Some of these signals help the immune system clear damaged cells. But others fuel chronic inflammation that can…
The new study challenges the conventional understanding of cellular senescence in cancer treatment. While many therapies push tumor cells into a state of senescence, where they stop dividing but do not die, these "undead" cells continue to release signals that can promote inflammation and further tumor growth. The study, published in Life Science Alliance, reveals that senescence is not a binary state but a dynamic trajectory, with different signaling molecules being released at different stages.
The researchers found that senescence unfolds in stages, with an early wave of tissue-remodeling signals followed weeks later by a delayed inflammatory response. They also discovered that different therapies can induce different forms of senescence, even when they appear to achieve the same end result. For instance, both chemotherapy and CDK4/6 inhibitors can induce an inflammatory response through the NF-κB pathway, but the CDK4/6 inhibitor takes a different route, starting with tissue remodeling before triggering inflammation.
The study also demonstrates that it is possible to suppress the inflammatory response without reversing the cells' growth arrest, potentially allowing researchers to harness the beneficial aspects of senescence while minimizing its harmful effects.
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