September 10, 2025EMBO ReportsOpen Access

STAT3 sustains tumorigenicity following mutant KRAS ablation

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STAT3 plays a critical role in sustaining tumor growth after mutant KRAS is inactivated.
Combined loss of mutant KRAS and STAT3 impairs tumor growth significantly in mice, enhancing immune rejection.
Cancer cells rely on STAT3 function to maintain oncogenic competence after CRISPR-mediated KRAS depletion.
This research identifies a key vulnerability in KRAS-ablated tumors linked to the STAT3 transcriptional program.

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Research reveals that STAT3 sustains tumorigenicity post-KRAS mutation ablation, suggesting new therapeutic targets.

D’Amico et al. (2025) studied this question.

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