Adamdec1-KO Mouse

ADAMDEC1, a disintegrin and metalloprotease domain-like protein, is a proteolytically active metzincin metalloprotease. It is involved in extracellular matrix remodeling, cell adhesion, invasion, and migration, and is associated with multiple signaling pathways including MMP2-related, Wnt/β -catenin, cAMP, and NF -κB signaling pathways [1,2,3,6]. It plays a crucial role in the pathogenesis of various diseases such as cancers (gliomas, colorectal cancer, cholangiocarcinoma, non -small cell lung cancer), pregnancy -related disorders (preeclampsia), and skin inflammation (rosacea) [1,2,3,4,6,7]. Genetic models, especially gene -knockout models, are valuable for studying its functions.

In gliomas, knockdown of ADAMDEC1 decreases cell proliferation, colony -forming ability, migration, and invasion, and induces apoptosis and G1 arrest, indicating its role in promoting glioma progression [1,5]. In colorectal cancer, ADAMDEC1 knockdown inhibits cell proliferation, migration, and invasion, and blocks epithelial -mesenchymal transition (EMT) by negatively regulating GSK -3β and inactivating the Wnt/β -catenin pathway [2]. In preeclampsia, a decrease in ADAMDEC1 might be involved in its development as interference to ADAMDEC1 impairs trophoblast differentiation [3]. In rosacea, knocking down ADAMDEC1 suppresses M1 macrophage polarization and skin inflammation [4]. In cholangiocarcinoma, ADAMDEC1 knockdown inhibits tumorigenicity and growth in vivo, and in non -small cell lung cancer, it decreases cell proliferation and colony -forming ability, and promotes apoptosis [6,7]. In atherosclerosis, ADAMDEC1 knockdown in human vascular smooth muscle cells suppresses cell proliferation and reduces the levels of MMP2 and MMP9 proteins [8].

In conclusion, ADAMDEC1 has diverse functions in multiple biological processes and disease conditions. Model -based research, particularly through gene -knockout models, has revealed its role in promoting the progression of various cancers, influencing pregnancy -related trophoblast differentiation, and contributing to skin inflammation and atherosclerosis. These findings highlight ADAMDEC1 as a potential therapeutic target for these diseases.

References:

1. Qi, Huimin, Wang, Ping, Sun, Hongliang, Dong, Junhong, Wang, Hongmei. 2022. ADAMDEC1 accelerates GBM progression via activation of the MMP2-related pathway. In Frontiers in oncology, 12, 945025. doi:10.3389/fonc.2022.945025. https://pubmed.ncbi.nlm.nih.gov/36172139/

2. Jia, Yuna, Huang, Xiaoyong, Shi, Haiyan, Han, Huihui, Zhang, Jing. 2023. ADAMDEC1 induces EMT and promotes colorectal cancer cells metastasis by enhancing Wnt/β-catenin signaling via negative modulation of GSK-3β. In Experimental cell research, 429, 113629. doi:10.1016/j.yexcr.2023.113629. https://pubmed.ncbi.nlm.nih.gov/37187249/

3. Li, Zhuo-Hang, Li, Xia, Li, Fang-Fang, Ding, Yu-Bin, Liu, Tai-Hang. . The roles of ADAMDEC1 in trophoblast differentiation during normal pregnancy and preeclampsia. In Molecular human reproduction, 28, . doi:10.1093/molehr/gaac014. https://pubmed.ncbi.nlm.nih.gov/35536241/

4. Liu, Tangxiele, Deng, Zhili, Xie, Hongfu, Zhao, Zhixiang, Li, Ji. 2019. ADAMDEC1 promotes skin inflammation in rosacea via modulating the polarization of M1 macrophages. In Biochemical and biophysical research communications, 521, 64-71. doi:10.1016/j.bbrc.2019.10.073. https://pubmed.ncbi.nlm.nih.gov/31627897/

5. Liu, Xueliang, Huang, Hao, Li, Xuehan, Zhang, Ye, Liu, Liang. 2020. Knockdown of ADAMDEC1 inhibits the progression of glioma in vitro. In Histology and histopathology, 35, 997-1005. doi:10.14670/HH-18-227. https://pubmed.ncbi.nlm.nih.gov/32378728/

6. Zhou, Shuo, Yang, Yuhang, Qi, Feiyu, Lu, Zheng, Chen, Yongliang. 2025. ADAMDEC1 promotes the malignant progression of cholangiocarcinoma by regulating NF-κB signaling pathway. In Scientific reports, 15, 817. doi:10.1038/s41598-025-85241-6. https://pubmed.ncbi.nlm.nih.gov/39755752/

7. Zhu, Weiliang, Shi, Lin, Gong, Yuxin, Zhang, Bei, Ke, Bin. 2022. Upregulation of ADAMDEC1 correlates with tumor progression and predicts poor prognosis in non-small cell lung cancer (NSCLC) via the PI3K/AKT pathway. In Thoracic cancer, 13, 1027-1039. doi:10.1111/1759-7714.14354. https://pubmed.ncbi.nlm.nih.gov/35178875/

8. Wang, Xiaochen, Gao, Feng, Cheng, Cheng, Zhang, Yanmei. 2023. Knockdown of ADAMDEC1 ameliorates ox-LDL-induced endothelial cell injury and atherosclerosis progression. In Functional & integrative genomics, 24, 1. doi:10.1007/s10142-023-01278-8. https://pubmed.ncbi.nlm.nih.gov/38063920/