FEN1 inhibition selectively impairs proliferation of colon cancer cells deficient in Cdc4 and Mre11a, both frequently mutated in colorectal cancers. FEN1 has also emerged as a potential chemosensitizing target due to its role in LP-BER since it is critical for repair of Methyl methanesulfonate-induced alkylation damage, and its knockdown or inhibition increases sensitivity to Temozolomide in glioblastoma and colorectal cancer cell lines[1].
Kinase Assay
Cell Assay
Animal Administration
References
[1]. Jack C Exell, et al. Cellularly Active N-hydroxyurea FEN1 Inhibitors Block Substrate Entry to the Active Site. Nat Chem Biol. 2016 Oct;12(10):815-21.
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