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Life sciences · Journal article
Nature Communications · October 24, 2026
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Immune evasion is a key driver of tumour evolution and a major barrier to effective cancer therapy, frequently arising through suppression of the cytosolic DNA-sensing cGAS–STING pathway. Here, we identify miR-30d as a post-transcriptional regulator that operates at two mechanistically distinct levels in breast cancer. Upstream, miR-30d maintains nuclear envelope integrity via the LATS2–YAP–Lamin B1 axis, limiting nuclear rupture, genomic damage, and cytosolic DNA leakage that activate cGAS. In parallel, miR-30d impairs STING trafficking from the endoplasmic reticulum to the Golgi, restraining TBK1 activation and downstream signal propagation. Inhibition of miR-30d restores cGAS activation and STING trafficking, enhancing type I interferon response and antitumour immunity, suppressing tumour growth, and improving responsiveness to immune checkpoint blockade. These findings define a miR-30d-regulated nuclear envelope–Golgi axis that restrains innate immune surveillance, and suggest miR-30d inhibition as a potential strategy to overcome immune evasion. Breast cancer cells use a short RNA molecule, miR-30d, to hide from immune attack by muting a cellular DNA-sensing alarm system. Blocking miR-30d reactivates the alarm, slows tumour growth and boosts immunotherapy.