Adam29-KO Mouse

ADAM29, a member of the membrane-anchored ADAM family of proteins, is highly expressed in testis and may mediate different physiological and pathological processes. It is a type I integral membrane protein that secretes a glycoprotein mediating cell-cell and cell-matrix interaction, with its abnormal expression involved in various physiological process diversifications [3,5].

In a mouse model, ADAM29 depletion does not affect mouse viability, development, or fertility, but it impacts metabolism and energy expenditure. Interestingly, ADAM29 deficiency leads to an accelerated wound-healing process without affecting cell reprogramming in mouse-derived fibroblasts [3].

In cancer research, ADAM29 shows increased expression in multiple cancers. In breast cancer, its increased transcript expression influences the proliferation, migration, and invasion of breast cancer cells in vitro [1]. In clear cell renal cell carcinoma (ccRCC), it promotes cell growth, invasion, and migration, and is positively correlated with proliferation-and motion-related proteins [2]. In esophageal squamous cell carcinoma (ESCC), its expression increases during the pathological evolution from normal epithelium to cancer, and is associated with tumor behavior characteristics and progression [4]. In gastric cancer, it promotes cell proliferation, migration, and invasion, and high expression is associated with poor patient survival [5]. In colon cancer, its expression is significantly higher in cancer tissues compared to normal tissues, and is regulated by hypomethylation and hyperacetylation [6].

In conclusion, ADAM29 is involved in cell-cell and cell-matrix interactions and various physiological processes. The gene knockout mouse model reveals its role in metabolism, energy expenditure, and wound healing. In cancer, it is associated with tumor development, progression, and patient prognosis in multiple cancer types, highlighting its potential as a prognostic factor and therapeutic target.

References:

1. Zhao, Meng, Jia, Wang, Jiang, Wen G, Cheng, Shan, Song, Maomin. . ADAM29 Expression in Human Breast Cancer and its Effects on Breast Cancer Cells In Vitro. In Anticancer research, 36, 1251-8. doi:. https://pubmed.ncbi.nlm.nih.gov/26977022/

2. Li, Shun-Lai, Jiang, Ting-Qi, Cao, Qing-Wei, Liu, Shan-Mei. 2020. Transmembrane protein ADAM29 facilitates cell proliferation, invasion and migration in clear cell renal cell carcinoma. In Journal of chemotherapy (Florence, Italy), 33, 40-50. doi:10.1080/1120009X.2020.1842035. https://pubmed.ncbi.nlm.nih.gov/33164721/

3. Campos-Iglesias, Diana, Montero, Alejandro A, Rodríguez, Francisco, López-Otín, Carlos, Freije, José M P. 2024. Loss of ADAM29 does not affect viability and fertility in mice but improves wound healing. In iScience, 27, 110135. doi:10.1016/j.isci.2024.110135. https://pubmed.ncbi.nlm.nih.gov/38966569/

4. Wang, Tingting, Lv, Xiaoyan, Jiang, Shen, Han, Shaorong, Wang, Yanming. 2020. Expression of ADAM29 and FAM135B in the pathological evolution from normal esophageal epithelium to esophageal cancer: Their differences and clinical significance. In Oncology letters, 19, 1727-1734. doi:10.3892/ol.2020.11272. https://pubmed.ncbi.nlm.nih.gov/32194665/

5. Chen, Hongbing, Wang, Siping. 2018. Clinical significance of ADAM29 promoting the invasion and growth of gastric cancer cells in vitro. In Oncology letters, 16, 1483-1490. doi:10.3892/ol.2018.8838. https://pubmed.ncbi.nlm.nih.gov/30008827/

6. Alrubie, Turki M, Shaik, Jilani P, Alamri, Abdullah M, Almaiman, Sarah M, Almutairi, Mikhlid H. 2023. FTHL17, PRM2, CABYR, CPXCR1, ADAM29, and CABS1 are highly expressed in colon cancer patients and are regulated in vitro by epigenetic alterations. In Heliyon, 10, e23689. doi:10.1016/j.heliyon.2023.e23689. https://pubmed.ncbi.nlm.nih.gov/38187237/