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Ataxia telangiectasia and Rad3-related (ATR) activates checkpoint kinase 1 (CHK1) following replication fork stalling, leading to cell cycle arrest. ATR-CHK1 pathway components are considered to be promising therapeutic targets to enhance the effectiveness of replication inhibitors. The present study revealed that F-Box protein 32 (FBXO32) regulated ATR expression in pancreatic cancer PANC-1 and MIA PaCa-2 cells. Additionally, FBXO32 interacts with ATR in PANC-1 cells and ATR is a degradation substrate of E3 ubiquitin ligase FBXO32. Furthermore, FBXO32 regulated the DNA damage response induced by gemcitabine in PANC-1 cells. Taken together, the results of the present study suggested that FBXO32, as an E3 ubiquitin ligase of ATR, regulates the DNA damage response induced by gemcitabine in pancreatic cancer.

3F‑Box protein 32 degrades ataxia telangiectasia and Rad3‑related and regulates DNA damage response induced by gemcitabine in pancreatic cancer