Authors
Yu-Xin Hua, Jie Gao, Qing-Qing Sun, Xiao-Min Wang, Jing-Yu Wang, Yuan Zhou, Long Zhang, Xian-Chao Zhang, Chun-Wei Xu, Bing Bao, Su-Ping Tao, Ying Xu, Wei-Wei Pan, Shu-Qun Cheng, Sheng-Bing Liu
Published in
NPJ precision oncology. Jul 13, 2026. Epub Jul 13, 2026.
Abstract
The Wnt/β-catenin pathway plays a critical role in colorectal cancer (CRC) development. The significance of Wnt/β-catenin in maintaining the stability of adult tissues and challenges in identifying suitable molecular targets have limited the application of targeting the Wnt/β-catenin pathway. As one of the Cullin RING Ligase 4 adapters, DNA damage-binding protein 1 (DDB1) - and CUL4 correlation factor 13 (DCAF13) appears strongly expressed in different tumors. Our findings confirm enhanced expression of DCAF13 in tissues of CRC origin and related cell. In colon cancer cells, DCAF13 regulated adenomatous polyposis coli membrane recruitment 2 (AMER2) through ubiquitination, DCAF13 deletion increased AMER2 expression, which inhibited Wnt/β-catenin activity, suppressing cell proliferation. This effect was further validated in mice with gut-specific DCAF13 knockout. The ubiquitin-proteasome system is a potential target for drug development and cancer treatment. Beta-propeller proteins, such as CRL4 adapter DCAFs, are easily targeted by drugs. DCAF-proteolysis-targeting chimeras (PROTACs) can overcome drug resistance and selectively target tumor drivers by leveraging the unique substrate specificity of the DCAF subunits. DCAF13 emerges as a promising target for CRC, acting via the DCAF13-AMER2-Wnt /β-catenin axis.
PMID:
42443527
Bibliographic data and abstract were imported from PubMed on 14 Jul 2026.
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