Ct45a, a gene with currently no widely-known common aliases, seems to be involved in multiple biological processes related to cancer. It may play a role in cell migration, epithelial-mesenchymal transition (EMT), stemness, and metastasis, and is associated with the AKT pathway [1].

In breast cancer cells, overexpression of UEV1A, a ubiquitin-E2 variant, induces CT45A family gene expression. Ectopic expression of UEV1A can stimulate CT45A and its downstream genes involved in tumorigenesis, EMT, stemness, and metastasis, promoting cell migration and EMT signaling. Depletion of CT45A abolishes these effects, indicating CT45A is a critical downstream effector of Uev1A. The Uev1A-induced cell migration and EMT signaling is dependent on AKT, suggesting CT45A acts downstream of the AKT pathway [1].

In non-small cell lung carcinoma (NSCLC), SMARCA4-truncated NSCLC shows enriched cancer/testis antigen (CTA) expression, with up to 57% of the cases displaying immunoreactivities for MAGEA4, CT45A, and/or PRAME. Increased CTA expression like CT45A could be a novel therapeutic target in SMARCA4-mutated NSCLCs [2].

In prostate cancer cell lines (PC-3 and DU145), the combinatory treatment of calcitriol and TGF-β down-regulates members of the CT45A family [3].

In a hemophilia A female, several novel X-linked gene mutations including CT45A were identified, though their impact on X-chromosome inactivation remains unclear [4].

In conclusion, Ct45a appears to be significantly involved in cancer-related biological processes, especially in breast cancer, NSCLC, and prostate cancer, as well as potentially in X-chromosome-related genetic disorders. The studies, including those related to gene expression manipulation (akin to gene knockout-like effects in some cases), have revealed its role in cell migration, EMT, and as a potential therapeutic target in certain cancers.

References:

1. Niu, Tong, Wu, Zhaojia, Xiao, Wei. 2021. Uev1A promotes breast cancer cell migration by up-regulating CT45A expression via the AKT pathway. In BMC cancer, 21, 1012. doi:10.1186/s12885-021-08750-3. https://pubmed.ncbi.nlm.nih.gov/34503444/

2. Ahn, Bokyung, Kim, Deokhoon, Ji, Wonjun, Jang, Se Jin, Hwang, Hee Sang. 2025. Clinicopathologic and genomic analyses of SMARCA4-mutated non-small cell lung carcinoma implicate the needs for tailored treatment strategies. In Lung cancer (Amsterdam, Netherlands), 201, 108445. doi:10.1016/j.lungcan.2025.108445. https://pubmed.ncbi.nlm.nih.gov/39954349/

3. García-Olivares, Mitzi, Romero-Córdoba, Sandra, Ortiz-Sánchez, Elizabeth, Larrea, Fernando, Barrera, David. 2021. Regulation of anti-tumorigenic pathways by the combinatory treatment of calcitriol and TGF-β in PC-3 and DU145 cells. In The Journal of steroid biochemistry and molecular biology, 209, 105831. doi:10.1016/j.jsbmb.2021.105831. https://pubmed.ncbi.nlm.nih.gov/33582304/

4. Tan, Xiaoyan, Yang, Yi, Wu, Xia, Chen, Shu, Lou, Shifeng. 2025. An investigation of a hemophilia A female with heterozygous intron 22 inversion and skewed X chromosome inactivation. In Frontiers in genetics, 15, 1500167. doi:10.3389/fgene.2024.1500167. https://pubmed.ncbi.nlm.nih.gov/39834547/