Rgs16, the regulator of G protein signaling 16, is a key factor in G protein-mediated activation. It plays a role in negatively controlling G protein-coupled receptor signal transduction pathways [3,9]. Rgs16 is associated with various biological processes and diseases, including cancer, neurodegenerative diseases, and cardiovascular diseases [3].

In cancer, Rgs16 has different effects. In tumors, it suppresses antitumor CD8+ T cell survival. Rgs16-deficient CD8+ T cells have inhibited apoptosis and enhanced antitumor effector functions, and Rgs16 deficiency can synergize with PD-1 blockade [1]. In esophageal cancer, knockdown of Rgs16 inhibits cell proliferation and migration by regulating Hippo-YAP activity [2]. In glioma, Rgs16 promotes progression, and its high expression is associated with poor prognosis [4,5]. In ulcerative colitis, Rgs16 expression in the colonic mucosa and peripheral blood mononuclear cells is increased and correlated with disease activity [6]. In macrophages, HBeAg upregulates Rgs16 expression, which then promotes macrophage activation and liver injury [7]. In monocytes, overexpression of Rgs16 reduces the expression of pro-inflammatory cytokines, while knockdown has the opposite effect [8]. In the lung, Rgs16-deficient mice show more robust granulomatous lung fibrosis and enhanced Th2/Th17 inflammatory responses [9].

In conclusion, Rgs16 is involved in multiple biological processes and diseases. Gene knockout models in mice have been crucial in revealing its role in cancer, inflammatory diseases, and immune-related responses. These findings provide insights into potential therapeutic strategies targeting Rgs16 for treating related diseases.

References:

1. Weisshaar, Nina, Wu, Jingxia, Ming, Yanan, Hofmann, Ilse, Cui, Guoliang. 2022. Rgs16 promotes antitumor CD8+ T cell exhaustion. In Science immunology, 7, eabh1873. doi:10.1126/sciimmunol.abh1873. https://pubmed.ncbi.nlm.nih.gov/35622904/

2. Zhang, Yanzhou, Zhu, Qing, Cao, Xiufeng, Ni, Bin. 2023. RGS16 regulates Hippo-YAP activity to promote esophageal cancer cell proliferation and migration. In Biochemical and biophysical research communications, 675, 122-129. doi:10.1016/j.bbrc.2023.04.033. https://pubmed.ncbi.nlm.nih.gov/37473526/

3. Wenbo, Liu, Liangyu, Xie, Zhiyong, Lu, Yuanzhen, Chen, Bin, Shi. . Status and trends of RGS16 based on data visualization analysis: A review. In Medicine, 103, e36981. doi:10.1097/MD.0000000000036981. https://pubmed.ncbi.nlm.nih.gov/38363937/

4. Wang, Chaochao, Xue, Hao, Zhao, Rongrong, Deng, Lin, Li, Gang. 2022. RGS16 regulated by let-7c-5p promotes glioma progression by activating PI3K-AKT pathway. In Frontiers of medicine, 17, 143-155. doi:10.1007/s11684-022-0929-y. https://pubmed.ncbi.nlm.nih.gov/36414916/

5. Huang, Ruoyu, Li, Guanzhang, Zhao, Zheng, Wang, Kuanyu, Hu, Huimin. 2020. RGS16 promotes glioma progression and serves as a prognostic factor. In CNS neuroscience & therapeutics, 26, 791-803. doi:10.1111/cns.13382. https://pubmed.ncbi.nlm.nih.gov/32319728/

6. Zhu, Fengqin, Qin, Yufen, Wang, Yan, Wang, Yibo, Zhou, Guangxi. 2022. Critical roles of RGS16 in the mucosal inflammation of ulcerative colitis. In European journal of gastroenterology & hepatology, 34, 993-999. doi:10.1097/MEG.0000000000002407. https://pubmed.ncbi.nlm.nih.gov/35830366/

7. Tian, Miaomiao, Wu, Nijin, Xie, Xiaoyu, Liu, Chenxi, Qi, Jianni. 2023. Phosphorylation of RGS16 at Tyr168 promote HBeAg-mediated macrophage activation by ERK pathway to accelerate liver injury. In Journal of molecular medicine (Berlin, Germany), 102, 257-272. doi:10.1007/s00109-023-02405-5. https://pubmed.ncbi.nlm.nih.gov/38141114/

8. Suurväli, J, Pahtma, M, Saar, R, Cavaillon, J M, Rüütel Boudinot, S. . RGS16 restricts the pro-inflammatory response of monocytes. In Scandinavian journal of immunology, 81, 23-30. doi:10.1111/sji.12250. https://pubmed.ncbi.nlm.nih.gov/25366993/

9. Shankar, Sucharita P, Wilson, Mark S, DiVietro, Jeffrey A, Wynn, Thomas A, Druey, Kirk M. 2012. RGS16 attenuates pulmonary Th2/Th17 inflammatory responses. In Journal of immunology (Baltimore, Md. : 1950), 188, 6347-56. doi:10.4049/jimmunol.1103781. https://pubmed.ncbi.nlm.nih.gov/22593615/