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Abstract

Copper is essential for cellular function, but excess copper is toxic, requiring tight regulation through copper‑binding proteins and the ATP7A and ATP7B transporters. While ATP7B’s role in hepatic copper export is well established, its functions in other tissues are less understood. This work examines ATP7B expression and trafficking in the human large intestine and ovary. In colonic epithelial cells, ATP7B localizes apically and undergoes copper‑dependent trafficking, supporting a model in which excess copper is packaged into vesicles and excreted into the intestinal lumen. Additionally, using cisplatin‑resistant A2780‑CP20 cells, we show that ATP7B does not traffic in response to copper or cisplatin, suggesting that resistance arises from intracellular binding and sequestration rather than ATP7B‑mediated drug efflux.

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