Smim24, whose full name is Small Integral Membrane Protein 24, likely plays a role in various biological processes based on the associated research. However, its exact core function, associated pathways, and overall biological importance are still being elucidated. Genetic models are valuable for further exploring its functions.

In clear-cell renal-cell carcinoma (ccRCC), Smim24 is part of a prognostic model related to activated dendritic cells. This model can predict outcomes, especially in advanced ccRCC patients, and is associated with tumor progression, tumor mutation burden, immune cell infiltration, and immunotherapy outcomes. Also, the expression of Smim24 in this context is correlated with sensitivity to JQ1, a BET inhibitor [1]. In another study on ccRCC, Smim24 is among the genes used to construct a prognostic model related to chemokine-related genes, with the high-risk group having a poorer prognosis [2]. In hepatocellular carcinoma, Smim24 is one of the nine overexpressed genes in CD13+CD166-cells that maintain tumorigenicity [3]. In the blood transcriptome of cognitively intact older adults, the expression of Smim24 shows longitudinal changes related to APOE4 status and amyloid accumulation, implicating disrupted immune system, protein removal, and metabolism [4]. In a case of 19p13.3 microduplication syndrome, Smim24 is within a duplicated chromosomal region, and this duplication may contribute to the patient's clinical phenotypes including nephrotic syndrome [5]. In clear cell renal carcinoma, Smim24 is part of a risk model based on Renin-angiotensin system related genes, which can predict prognosis and drug sensitivity [6].

In summary, Smim24 appears to be involved in cancer-related processes such as tumorigenicity and prognosis prediction in ccRCC and hepatocellular carcinoma. It may also be associated with neurodegenerative-related mechanisms in relation to APOE4 and amyloid, as well as contribute to the clinical phenotypes in 19p13.3 microduplication syndrome. The study of Smim24 through various genetic models helps in understanding its role in these disease areas.

References:

1. Ye, Zijian, Zhang, Yifan, Xu, Jialiang, Wang, Meijiao, Xie, Biao. 2024. Integrating Bulk and Single-Cell RNA-Seq Data to Identify Prognostic Features Related to Activated Dendritic Cells in Clear-Cell Renal-Cell Carcinoma. In International journal of molecular sciences, 25, . doi:10.3390/ijms25179235. https://pubmed.ncbi.nlm.nih.gov/39273185/

2. Meng, Yuhao, Zhang, Chen, Fu, Tongfei, Wu, Junsong, Zhan, Yongli. 2024. Exploring the tumor microenvironment: Chemokine-related genes and immunotherapy/chemotherapy response in clear-cell renal cell carcinoma. In Environmental toxicology, , . doi:10.1002/tox.24190. https://pubmed.ncbi.nlm.nih.gov/38488671/

3. Seyama, Yusuke, Sudo, Kazuhiro, Hirose, Suguru, Tsuchiya, Kiichiro, Nakamura, Yukio. 2023. Identification of a gene set that maintains tumorigenicity of the hepatocellular carcinoma cell line Li-7. In Human cell, 36, 2074-2086. doi:10.1007/s13577-023-00967-7. https://pubmed.ncbi.nlm.nih.gov/37610679/

4. Luckett, Emma S, Zielonka, Magdalena, Kordjani, Amine, Cleynen, Isabelle, Vandenberghe, Rik. 2023. Longitudinal APOE4- and amyloid-dependent changes in the blood transcriptome in cognitively intact older adults. In Alzheimer's research & therapy, 15, 121. doi:10.1186/s13195-023-01242-5. https://pubmed.ncbi.nlm.nih.gov/37438770/

5. Sun, Wenjie, Yan, Hong, Sun, Mengxin, Wang, Jie, Li, Kunxia. 2025. Expanding the clinical spectrum of 19p13.3 microduplication syndrome: a case report highlighting nephrotic syndrome and literature review. In BMC pediatrics, 25, 70. doi:10.1186/s12887-025-05394-1. https://pubmed.ncbi.nlm.nih.gov/39875952/

6. Chang, Qinzheng, Zhao, Shuo, Sun, Jiajia, Fan, Yidong, Liu, Jikai. 2025. Identification of a novel prognostic and therapeutic prediction model in clear cell renal carcinoma based on Renin-angiotensin system related genes. In Frontiers in endocrinology, 16, 1521940. doi:10.3389/fendo.2025.1521940. https://pubmed.ncbi.nlm.nih.gov/40099255/