TRIM52, a member of the tripartite motif (TRIM) family, is an E3 ubiquitin ligase. It has been implicated in regulating various biological functions, with a notable role in activating the NF-κB signaling pathway, and is thus involved in processes like cell proliferation, apoptosis, inflammation, and pyroptosis. These functions make it biologically important in understanding normal cellular processes and disease mechanisms [7].

Knockdown of TRIM52 in ovarian cancer cell lines (SKOV3 and CAOV3) inhibited cell invasion, migration, and proliferation, and induced apoptosis. It also downregulated the mRNA and protein levels of NF-κB downstream effectors and upregulated caspase-3. In nude mice, knockdown of TRIM52 blocked tumor growth [1]. In colorectal cancer cell lines (SW480 and LoVo), short hairpin RNAs targeting TRIM52 had anti-proliferative effects by inducing apoptosis, and in vivo xenograft experiments confirmed these results [2]. In dextran sulfate sodium-induced inflammatory bowel disease in mice, knockdown of TRIM52 alleviated symptoms, retarded the inflammatory response, and inhibited pyroptosis in colon tissue [3]. In lung cancer cells, downregulation of TRIM52 suppressed cell proliferation, arrested the cell cycle at the G1 phase, and counteracted the effects of the Wnt/β-catenin pathway [4]. In IL-1β-induced synovial fibroblasts, knockdown of TRIM52 relieved cell proliferation, inflammatory response, and oxidative stress [5]. In human benign prostatic hyperplasia cells (BPH-1), silencing TRIM52 suppressed cell growth and decreased the promoter activity of NF-κB [6]. In colon cancer cells, knockdown of TRIM52 inhibited cell proliferation, migration, invasion, and promoted apoptosis, and was related to the activation of the NF-κB signaling pathway [8].

In conclusion, TRIM52 plays oncogenic roles in multiple cancers such as ovarian, colorectal, lung, and colon cancer, and promotes inflammation and pyroptosis in inflammatory bowel disease. These functions are often mediated through the activation of the NF-κB signaling pathway, as demonstrated by various knockdown experiments in cell lines and in vivo models. The study of TRIM52 knockdown models provides valuable insights into its role in these disease conditions, potentially guiding the development of targeted therapies [1-6, 8].

References:

1. Yang, Weihong, Liu, Li, Li, Caixia, Yu, Fudong, Cheng, Zhongping. 2018. TRIM52 plays an oncogenic role in ovarian cancer associated with NF-kB pathway. In Cell death & disease, 9, 908. doi:10.1038/s41419-018-0881-6. https://pubmed.ncbi.nlm.nih.gov/30185771/

2. Pan, Shengli, Deng, Yingying, Fu, Jun, Ru, Xiaokun, Qin, Xianju. 2019. TRIM52 promotes colorectal cancer cell proliferation through the STAT3 signaling. In Cancer cell international, 19, 57. doi:10.1186/s12935-019-0775-4. https://pubmed.ncbi.nlm.nih.gov/30918473/

3. Ma, Jin-Ping, Yao, Cheng-Zi, Jia, Zhi-Qiang, Gao, Xiang-Xiang, Su, Li-Ping. 2023. TRIM52 aggravated inflammation and pyroptosis in dextran sulfate sodium-induced inflammatory bowel disease through activation of the TLR4/NF-κBs pathway. In Allergologia et immunopathologia, 51, 159-167. doi:10.15586/aei.v51i1.737. https://pubmed.ncbi.nlm.nih.gov/36617836/

4. Mu, Xiaoyan, Li, Hegen, Zhou, Lei, Xu, Weijie. 2019. TRIM52 regulates the proliferation and invasiveness of lung cancer cells via the Wnt/β‑catenin pathway. In Oncology reports, 41, 3325-3334. doi:10.3892/or.2019.7110. https://pubmed.ncbi.nlm.nih.gov/31002351/

5. Ma, Tie, Wu, Chuan-Bin, Shen, Qing-Xia, Wang, Qiang, Zhou, Qing. . TRIM52 knockdown inhibits proliferation, inflammatory responses and oxidative stress in IL-1β-induced synovial fibroblasts to alleviate temporomandibular joint osteoarthritis. In Journal of cellular and molecular medicine, 28, e18244. doi:10.1111/jcmm.18244. https://pubmed.ncbi.nlm.nih.gov/38520211/

6. Sun, Jianming, Liu, Peng, Mao, Jianmin, Jiang, Xiaomei, Gu, Yin. 2020. TRIM52 positively mediates NF-κB to promote the growth of human benign prostatic hyperplasia cells through affecting TRAF2 ubiquitination. In Life sciences, 259, 118380. doi:10.1016/j.lfs.2020.118380. https://pubmed.ncbi.nlm.nih.gov/32898524/

7. Fan, Wenchun, Liu, Tingting, Li, Xiangmin, Chen, Huanchun, Qian, Ping. 2017. TRIM52: A nuclear TRIM protein that positively regulates the nuclear factor-kappa B signaling pathway. In Molecular immunology, 82, 114-122. doi:10.1016/j.molimm.2017.01.003. https://pubmed.ncbi.nlm.nih.gov/28073078/

8. Guo, Yanjiao, Zhou, Yiming, Gu, Xiaodong, Xiang, Jianbin. . Tripartite motif 52 (TRIM52) promotes proliferation, migration, and regulation of colon cancer cells associated with the NF-κB signaling pathway. In Journal of gastrointestinal oncology, 13, 1097-1111. doi:10.21037/jgo-22-317. https://pubmed.ncbi.nlm.nih.gov/35837156/