Abstract

In this issue of Cancer Research, Ranoa and colleagues report on the role of STING (stimulator of IFN genes, TMEM173) in regulating critical tumor cell-intrinsic functions including cell-cycle progression, chromosomal stability, and cellular response to therapeutic ionizing radiation. The authors used multiple methods including RNA expression profiling, molecular and biochemical techniques, cell biology, and reagents from genetically modified murine models to test their hypothesis that downregulating the STING pathway in cancer cells promotes cellular transformation through accumulation of chromosomal instability and premature progression of the cell cycle. Their findings demonstrate that STING is a tumor suppressor that inhibits cell proliferation by restricting entry to mitosis as well as protecting cells against aneuploidy. These findings significantly advance our understanding of the role of STING as a tumor gate keeper.See related article by Ranoa et al., p. 1465.

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