C1ORF112在肝细胞癌中的表达、功能及临床意义研究进展
Research Progress on the Expression, Function and Clinical Significance of C1ORF112 in Hepatocellular Carcinoma
DOI: 10.12677/acm.2026.1693186, PDF,   
作者: 伍寿千, 李宇凡:绍兴大学医学院,浙江 绍兴;萧 岗*:绍兴市人民医院肝胆外科,浙江 绍兴
关键词: C1ORF112;肝细胞癌;生物标志物;预后;DNA损伤修复;靶向治疗;C1ORF112; Hepatocellular Carcinoma; Biomarker; Prognosis; DNA Damage Repair; Targeted Therapy
摘要: 目的:系统梳理染色体1开放阅读框112 (C1ORF112)在肝细胞癌(HCC)中的表达特征、临床预后价值及分子机制研究进展,评估其作为新型生物标志物和潜在治疗靶点的可行性。方法:检索PubMed、Web of Science、CNKI等数据库中关于C1ORF112与肝细胞癌的相关文献,对现有证据进行归纳、整合与评述。结果:C1ORF112在HCC组织中普遍高表达,其表达水平与肿瘤病理分期呈显著正相关,且高表达患者的总生存期明显缩短。约8%的HCC患者存在C1ORF112基因拷贝数扩增,扩增与较差的无进展生存期和无病生存期显著相关。在分子层面,C1ORF112与RAD51、FIGNL1等DNA修复相关蛋白相互作用,其共表达基因富集于细胞周期和有丝分裂调控通路。结论:C1ORF112有望成为HCC的新型预后生物标志物和潜在治疗靶点。然而,目前尚缺乏针对HCC的大规模前瞻性临床验证及体内功能研究,其具体调控网络和临床转化路径仍需深入探索。
Abstract: Objectives: To systematically review the expression characteristics, clinical prognostic value, and molecular mechanisms of Chromosome 1 Open Reading Frame 112 (C1ORF112) in hepatocellular carcinoma (HCC), and to evaluate its feasibility as a novel biomarker and potential therapeutic target. Methods: Relevant literature on C1ORF112 and HCC was retrieved from PubMed, Web of Science, and CNKI databases, and the available evidence was summarized, integrated, and critically appraised. Results: C1ORF112 is commonly overexpressed in HCC tissues, and its expression level is significantly positively correlated with pathological stage. Patients with high C1ORF112 expression have significantly shorter overall survival. Approximately 8% of HCC patients harbor C1ORF112 gene copy number amplification, which is significantly associated with worse progression-free survival and disease-free survival. At the molecular level, C1ORF112 physically interacts with DNA repair-related proteins including RAD51 and FIGNL1, and its co-expressed genes are enriched in cell cycle and mitotic regulation pathways. Conclusions: C1ORF112 holds promise as a novel prognostic biomarker and potential therapeutic target for HCC. However, large-scale prospective clinical validation and in vivo functional studies specifically for HCC are still lacking, and the precise regulatory networks and translational pathways require further investigation.
文章引用:伍寿千, 李宇凡, 萧岗. C1ORF112在肝细胞癌中的表达、功能及临床意义研究进展[J]. 临床医学进展, 2026, 16(9): 1474-1480. https://doi.org/10.12677/acm.2026.1693186

参考文献

[1] Zheng, J. and Gong, J. (2025) SLC1A4 Promotes Malignant Transformation of Hepatocellular Carcinoma by Activating the AKT Signaling. Analytical Cellular Pathology, 2025, Article ID: 1115184.
https://doi.org/10.1155/ancp/1115184
[2] Fan, F., Wu, H., Liu, Z., Hou, X., Chen, W., Wang, A., et al. (2016) Nuclear PKM2 Expression, an Independent Risk Factor for ER after Curative Resection of Hepatocellular Carcinoma. Biomedicine & Pharmacotherapy, 84, 1858-1864.
https://doi.org/10.1016/j.biopha.2016.10.108
[3] Hu, J., Wang, N., Yang, Y., Ma, L., Han, R., Zhang, W., et al. (2018) Diagnostic Value of Alpha-Fetoprotein Combined with Neutrophil-to-Lymphocyte Ratio for Hepatocellular Carcinoma. BMC Gastroenterology, 18, Article No. 186.
https://doi.org/10.1186/s12876-018-0908-6
[4] Chi, X., Jiang, L., Yuan, Y., Huang, X., Yang, X., Hochwald, S., et al. (2022) A Comparison of Clinical Pathologic Characteristics between Alpha-Fetoprotein Negative and Positive Hepatocellular Carcinoma Patients from Eastern and Southern China. BMC Gastroenterology, 22, Article No. 202.
https://doi.org/10.1186/s12876-022-02279-w
[5] Xu, Y., Guo, Q. and Wei, L. (2021) The Emerging Influences of Alpha-Fetoprotein in the Tumorigenesis and Progression of Hepatocellular Carcinoma. Cancers, 13, Article 5096.
https://doi.org/10.3390/cancers13205096
[6] Chen, J., Mai, H., Chen, H., Zhou, B., Hou, J. and Jiang, D. (2021) Pan-Cancer Analysis Identified C1ORF112 as a Potential Biomarker for Multiple Tumor Types. Frontiers in Molecular Biosciences, 8, Article 693651.
https://doi.org/10.3389/fmolb.2021.693651
[7] Kramvis, A., Chang, K., Dandri, M., Farci, P., Glebe, D., Hu, J., et al. (2022) A Roadmap for Serum Biomarkers for Hepatitis B Virus: Current Status and Future Outlook. Nature Reviews Gastroenterology & Hepatology, 19, 727-745.
https://doi.org/10.1038/s41575-022-00649-z
[8] Grinspan, L.T. and Villanueva, A. (2022) Biomarker Development Using Liquid Biopsy in Hepatocellular Carcinoma. Seminars in Liver Disease, 42, 188-201.
https://doi.org/10.1055/s-0042-1748924
[9] Edogbanya, J., Tejada‐Martinez, D., Jones, N.J., Jaiswal, A., Bell, S., Cordeiro, R., et al. (2021) Evolution, Structure and Emerging Roles of C1ORF112 in DNA Replication, DNA Damage Responses, and Cancer. Cellular and Molecular Life Sciences, 78, 4365-4376.
https://doi.org/10.1007/s00018-021-03789-8
[10] Wang, Y. and Deng, B. (2023) Hepatocellular Carcinoma: Molecular Mechanism, Targeted Therapy, and Biomarkers. Cancer and Metastasis Reviews, 42, 629-652.
https://doi.org/10.1007/s10555-023-10084-4
[11] Liu, J., Park, K., Shen, Z., Lee, H., Geetha, P., Pakyari, M., et al. (2023) Immunotherapy, Targeted Therapy, and Their Cross Talks in Hepatocellular Carcinoma. Frontiers in Immunology, 14, Article 1285370.
https://doi.org/10.3389/fimmu.2023.1285370
[12] Tischler, J.D., Tsuchida, H., Bosire, R., Oda, T.T., Park, A. and Adeyemi, R.O. (2024) FLIP (C1orf112)-FIGNL1 Complex Regulates RAD51 Chromatin Association to Promote Viability after Replication Stress. Nature Communications, 15, Article No. 866.
https://doi.org/10.1038/s41467-024-45139-9
[13] Zhou, Z., Yang, H., Liang, X., Zhou, T., Zhang, T., Yang, Y., et al. (2023) C1orf112 Teams up with FIGNL1 to Facilitate RAD51 Filament Disassembly and DNA Interstrand Cross-Link Repair. Cell Reports, 42, Article ID: 112907.
https://doi.org/10.1016/j.celrep.2023.112907
[14] Mazouzi, A., Moser, S.C., Abascal, F., van den Broek, B., Del Castillo Velasco-Herrera, M., van der Heijden, I., et al. (2023) FIRRM/C1orf112 Mediates Resolution of Homologous Recombination Intermediates in Response to DNA Interstrand Crosslinks. Science Advances, 9, eadf4409.
https://doi.org/10.1126/sciadv.adf4409
[15] Stok, C., Tsaridou, S., van den Tempel, N., Everts, M., Wierenga, E., Bakker, F.J., et al. (2023) FIRRM/C1orf112 Is Synthetic Lethal with PICH and Mediates RAD51 Dynamics. Cell Reports, 42, Article ID: 112668.
https://doi.org/10.1016/j.celrep.2023.112668
[16] Wang, J., Yang, G., Deng, X., Liu, X., Chen, D. and Liu, Q. (2026) C1ORF112 Drives Lung Adenocarcinoma Progression through E2F8-Mediated Transcriptional Activation. Journal of Thoracic Disease, 18, 606-606.
https://doi.org/10.21037/jtd-2026-1-0085
[17] Wang, L., Meng, X., Sun, Y., Ren, S., Lan, Y. and Tang, L. (2025) Molecular Mechanisms by Which C1orf112 Promotes Endometrial Cancer Progression and the Development and Validation of a Clinical Scoring Model. Clinical Epigenetics, 17, Article No. 188.
https://doi.org/10.1186/s13148-025-02003-x
[18] Zhang, Z., Tan, Z., Lv, Q., Wang, L., Yu, K., Yang, H., et al. (2021) High Expression of C1ORF112 Predicts a Poor Outcome: A Potential Target for the Treatment of Low-Grade Gliomas. Frontiers in Genetics, 12, Article 710944.
https://doi.org/10.3389/fgene.2021.710944
[19] Testa, U., Castelli, G. and Pelosi, E. (2024) Recent Developments in Molecular Targeted Therapies for Hepatocellular Carcinoma in the Genomic Era. Expert Review of Molecular Diagnostics, 24, 803-827.
https://doi.org/10.1080/14737159.2024.2392278
[20] Gujarathi, R., Franses, J.W., Pillai, A. and Liao, C. (2024) Targeted Therapies in Hepatocellular Carcinoma: Past, Present, and Future. Frontiers in Oncology, 14, Article 1432423.
https://doi.org/10.3389/fonc.2024.1432423