Agbl2-KO Mouse

AGBL2, short for ATP/GTP binding protein like 2, has been reported to catalyze α-tubulin detyrosination, which is involved in processes like cell proliferation and migration, and is associated with multiple biological pathways including signal transduction and immune infiltration [1,2,3]. It has potential importance in various biological processes and diseases, and genetic models could be valuable for further exploring its functions.

In renal cell carcinoma (RCC), TCGA analysis showed increased AGBL2 expression in patients, correlated with poorer survival. Knockdown of AGBL2 in RCC cells inhibited cell proliferation and migration, while overexpression increased these activities. AGBL2 also enhanced AKT phosphorylation in RCC cells [1].

In hepatocellular carcinoma (HCC), AGBL2 was frequently overexpressed in tissues and cell lines. Overexpression of AGBL2 promoted HCC cell survival, proliferation in vitro and tumor growth in vivo, inhibited apoptosis through enhancing IRGM-regulated autophagy, and up-regulated TPX2 and Aurora A activity to promote cell proliferation [2].

In ovarian carcinoma, high AGBL2 expression was associated with tumor histological grade, advanced stages, and shorter patient survival, and was identified as an independent prognostic factor [3].

In breast and gastric cancer, AGBL2 was related to clinicopathological parameters, prognosis, and cell proliferation and chemotherapy resistance, and it formed immune complexes with its inhibitor latexin [4,5].

In conclusion, AGBL2 plays a crucial role in promoting cell proliferation, migration, and tumor growth in multiple cancers including RCC, HCC, ovarian, breast, and gastric cancer. The study of AGBL2 in these contexts using model-based research, such as knockdown experiments in cell lines, has provided insights into its functions in disease development, potentially guiding the identification of new prognostic markers and therapeutic targets.

References:

1. Liu, Wei, Zhang, Yifei, Nie, Yechen, Gong, Binbin, Ma, Ming. 2024. AGBL2 promotes renal cell carcinoma cells proliferation and migration via α-tubulin detyrosination. In Heliyon, 10, e37086. doi:10.1016/j.heliyon.2024.e37086. https://pubmed.ncbi.nlm.nih.gov/39315218/

2. Wang, Li-Li, Jin, Xiao-Han, Cai, Mu-Yan, Liu, Fang, Xie, Dan. 2017. AGBL2 promotes cancer cell growth through IRGM-regulated autophagy and enhanced Aurora A activity in hepatocellular carcinoma. In Cancer letters, 414, 71-80. doi:10.1016/j.canlet.2017.11.003. https://pubmed.ncbi.nlm.nih.gov/29126912/

3. He, Wei-Peng, Wang, Li-Li. 2019. High expression of AGBL2 is a novel prognostic factor of adverse outcome in patients with ovarian carcinoma. In Oncology letters, 18, 4900-4906. doi:10.3892/ol.2019.10829. https://pubmed.ncbi.nlm.nih.gov/31612000/

4. Zhang, Hao, Ren, Yuan, Pang, Deyan, Liu, Caigang. 2014. Clinical implications of AGBL2 expression and its inhibitor latexin in breast cancer. In World journal of surgical oncology, 12, 142. doi:10.1186/1477-7819-12-142. https://pubmed.ncbi.nlm.nih.gov/24884516/

5. Zhu, Haitao, Zheng, Zhichao, Zhang, Jianjun, Su, Xiaohui, Gu, Xiaohu. . Effects of AGBL2 on cell proliferation and chemotherapy resistance of gastric cancer. In Hepato-gastroenterology, 62, 497-502. doi:. https://pubmed.ncbi.nlm.nih.gov/25916089/