Researchers mapped a USP11–IGF2BP2–ATOX1 molecular axis that shields non-small cell lung cancer cells from copper-driven cuproptosis. By identifying the pathway that preserves cell survival under copper stress, the work points to new drug targets that could restore vulnerability. The finding ties a specific signaling/effector chain to resistance, offering a mechanistic alternative to purely biomarker-driven strategies in the effort to expand copper-dependent cell death approaches.
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