Lung tumor microenvironment established by simultaneous activation of KrasG12D and deletion of neddylation conjugation enzyme UBE2M
Peer-Reviewed Publication
Updates every hour. Last Updated: 28-Oct-2026 22:17 ET (29-Oct-2026 02:17 GMT/UTC)
A research team led by Prof. Yi Sun at Zhejiang University, reported a unexpected finding that the combination of KrasG12D activation and genetic inactivation of UBE2M in the lung triggers the cGAS-STING-NF-κB signal to form a inflammatory tumor microenvironment (TME). Mechnistically, KrasG12D promotes the mitochondrial biogenesis, whereas UBE2M depletion inhibits Parkin neddylation and mitophagy, together causing the cytoplasmic release of damaged mitochondrial DNA. The STING antagonist H-151 rescues TME, indicating a causal role of the cGAS-STING signal. The study therefore demonstrates a unexpected role of UBE2M in prevention TME induced by Kras mutant.
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