C1orf112 promotes breast cancer growth by modulating the cell cycle

Background C1orf112 (Chromosome 1 Open Reading Frame 112) is involved in DNA damage repair, and its abnormal expression has been implicated in multiple cancers, including breast cancer. This study explores the function of C1orf112 in breast cancer through bioinformatics and experimental validation. Methods C1orf112 expression in breast cancer was analyzed using TCGA and HPA databases. Diagnostic efficiency was assessed using receiver operating characteristic (ROC) curves, and its prognostic significance was evaluated via KM plotter and TCGA data. GO and KEGG analyses were performed to explore potential mechanisms. Experimental validation included qRT-PCR and immunohistochemistry to confirm expression levels in breast cancer cells and tissues. Function assays, including CCK-8, colony formation and flow cytometry were conducted to assess the impact of C1orf112 on cell proliferation, cycle progression, and apoptosis. Results C1orf112 was highly expressed in breast cancer, with bioinformatics and immunohistochemical analysis confirming its upregulation in tumor tissues as its potential as a diagnostic marker. Functional enrichment analysis linked C1orf112 overexpression to cell proliferation-related pathways. Immunohistochemistry revealed associations between C1orf112 expression and ER-positive status, HER2 status, and molecular subtypes. Cellular assays demonstrated that C1orf112 promotes breast cancer proliferation by influencing cell cycle regulation, involving key molecules such as CCNB1 (cyclin B1). In vivo experiments further confirmed these effects. Conclusion C1orf112 contributes to breast cancer progression in association with cell cycle pathways, making it a potential diagnostic and therapeutic target with clinical applications.