The potential mechanisms underlying the effects of cGAS on TNBC metastasis.

Recent reports have revealed that high chromosomal instability or the cGAMP produced by cancer cells induces STING activation and triggers atypical NF-kB signaling and inflammatory responses, which promote cancer metastasis in a cell-autonomous or non-cell-autonomous fashion, suggesting that the cGAS-STING signaling may have dual roles in cancer progression. However, cGAS has also been found to suppress homologous-recombination-mediated repair and induce genomic instability upon DNA damage, arguing that the function of cGAS in tumorigenesis may not depend on STING signaling, but its exact functions and mechanisms in the metastasis of vast majority of cancer cells with moderate CIN remain largely unclear.