结直肠癌
生物
内科学
癌症研究
生物信息学
医学
癌症
作者
Jinghua Cao,Chenhui Cao,Jin‐Long Lin,Siyu Li,Longjun He,Kai Han,Jiewei Chen,Si Li,Xin Wang,Dan Xie,Feng‐Wei Wang
出处
期刊:Cell Reports
[Elsevier]
日期:2024-01-01
卷期号:43 (1): 113654-113654
被引量:1
标识
DOI:10.1016/j.celrep.2023.113654
摘要
Summary
Deficiency of DNA repair pathways drives the development of colorectal cancer. However, the role of the base excision repair (BER) pathway in colorectal cancer initiation remains unclear. This study shows that Nei-like DNA glycosylase 1 (NEIL1) is highly expressed in colorectal cancer (CRC) tissues and associated with poorer clinical outcomes. Knocking out neil1 in mice markedly suppresses tumorigenesis and enhances infiltration of CD8+ T cells in intestinal tumors. Furthermore, NEIL1 directly forms a complex with SATB2/c-Myc to enhance the transcription of COL17A1 and subsequently promotes the production of immunosuppressive cytokines in CRC cells. A NEIL1 peptide suppresses intestinal tumorigenesis in ApcMin/+ mice, and targeting NEIL1 demonstrates a synergistic suppressive effect on tumor growth when combined with a nuclear factor κB (NF-κB) inhibitor. These results suggest that combined targeting of NEIL1 and NF-κB may represent a promising strategy for CRC therapy.
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