Nup37, a member of the nucleoporin family, is a component of the nuclear pore complex (NPC) that serves as a crucial channel between the nucleus and cytoplasm, regulating the shuttling of proteins [5]. It has been implicated in various biological processes, and its dysregulation is associated with multiple diseases, especially cancer [1-6].

In hepatocellular carcinoma (HCC), Nup37 silencing suppressed lipid synthesis, cell proliferation, migration, and invasion in vitro, and restrained tumor growth in xenograft mouse models in vivo [1]. In glioma cells, the expression level of Nup37 affects proliferation and invasion, and overexpression of DNMT1 can alleviate the adverse effects caused by Nup37 depletion [2]. In non-small cell lung cancer cells, knockdown of Nup37 suppressed cell growth and proliferation, induced G1 phase cell cycle arrest and apoptosis [3]. In breast cancer cells, down-regulation of Nup37 inhibited cell growth, migration, and stemness [4]. In colon cancer cells, silencing of DEPDC1B, which regulates Nup37, inhibited cell proliferation, migration, invasion, and promoted apoptosis and cell cycle arrest, and Nup37 overexpression reversed these effects [6].

In conclusion, Nup37 plays significant roles in promoting the progression of multiple cancers, including HCC, glioma, non-small cell lung cancer, breast cancer, and colon cancer. Gene-knockout or knockdown models of Nup37 in these cancer types have revealed its oncogenic functions, suggesting it could be a potential biomarker and therapeutic target for these diseases [1-5, 9].

References:

1. Liu, Zhiyi, Hu, Qinghe, Luo, Qing, Shi, Hengliang, Zhang, Bin. 2024. NUP37 accumulation mediated by TRIM28 enhances lipid synthesis to accelerate HCC progression. In Oncogene, 43, 3255-3267. doi:10.1038/s41388-024-03167-1. https://pubmed.ncbi.nlm.nih.gov/39294431/

2. Lv, Yongqiang, Wang, Chaolian, Liu, Ruoyu, Jiang, Tianwei, Chen, Lujun. 2024. NUP37 promotes the proliferation and invasion of glioma cells through DNMT1-mediated methylation. In Cell death discovery, 10, 373. doi:10.1038/s41420-024-02138-5. https://pubmed.ncbi.nlm.nih.gov/39174498/

3. Huang, Lianglong, Wang, Tao, Wang, Fumu, Zhang, Licheng, Li, Yuping. 2020. NUP37 silencing induces inhibition of cell proliferation, G1 phase cell cycle arrest and apoptosis in non-small cell lung cancer cells. In Pathology, research and practice, 216, 152836. doi:10.1016/j.prp.2020.152836. https://pubmed.ncbi.nlm.nih.gov/32014308/

4. Li, Kangdi, Liu, Ting. 2021. Evaluation of Oncogene NUP37 as a Potential Novel Biomarker in Breast Cancer. In Frontiers in oncology, 11, 669655. doi:10.3389/fonc.2021.669655. https://pubmed.ncbi.nlm.nih.gov/34386417/

5. Luo, Xiaoling, Liu, Yuting, Feng, Weiguang, Wu, Jinsheng, Wang, Shaochuang. 2017. NUP37, a positive regulator of YAP/TEAD signaling, promotes the progression of hepatocellular carcinoma. In Oncotarget, 8, 98004-98013. doi:10.18632/oncotarget.20336. https://pubmed.ncbi.nlm.nih.gov/29228669/

6. Xiong, Hui, Li, Yun, Liu, Manhua. 2023. DEPDC1B is involved in the proliferation, metastasis, cell cycle arrest and apoptosis of colon cancer cells by regulating NUP37. In Molecular medicine reports, 27, . doi:10.3892/mmr.2023.13013. https://pubmed.ncbi.nlm.nih.gov/37203403/