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- W4286002146 abstract "DNA damage repair plays a key role in maintaining genomic stability and integrity. Flap endonuclease 1 (FEN1) is a core protein in the base excision repair (BER) pathway and participates in Okazaki fragment maturation during DNA replication. Several studies have implicated FEN1 in the regulation of other DNA repair pathways, including homologous recombination repair (HRR) and non-homologous end joining (NHEJ). Abnormal expression or mutation of FEN1 in cells can cause a series of pathological responses, leading to various diseases, including cancers. Moreover, overexpression of FEN1 contributes to drug resistance in several types of cancers. All this supports the hypothesis that FEN1 could be a therapeutic target for cancer treatment. Targeting FEN1 has been verified as an effective strategy in mono or combined treatment of cancer. Small-molecule compounds targeting FEN1 have also been developed and detected in cancer regression. In this review, we summarize the recent development of small-molecule inhibitors targeting FEN1 in recent years, thereby expanding their therapeutic potential and application." @default.
- W4286002146 created "2022-07-21" @default.
- W4286002146 creator A5060922308 @default.
- W4286002146 creator A5071297926 @default.
- W4286002146 creator A5071560765 @default.
- W4286002146 date "2022-07-20" @default.
- W4286002146 modified "2023-10-14" @default.
- W4286002146 title "Small-Molecule Inhibitors Targeting FEN1 for Cancer Therapy" @default.
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- W4286002146 doi "https://doi.org/10.3390/biom12071007" @default.
- W4286002146 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/35883563" @default.
- W4286002146 hasPublicationYear "2022" @default.
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