ORIGINAL RESEARCH article
Front. Bioeng. Biotechnol.
Sec. Cell and Gene Therapy
C1orf112 Promotes Breast Cancer Growth by Modulating the Cell Cycle
Provisionally accepted
- Tongji Hospital Affiliated to Tongji University, Shanghai, China
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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. Conclusions: C1orf112 contributes to breast cancer progression in association with cell cycle pathways, making it a potential diagnostic and therapeutic target with clinical applications.
Keywords: Apoptosis, breast cancer, C1ORF112, prognosis, proliferation
Received: 10 Oct 2025; Accepted: 16 Feb 2026.
Copyright: © 2026 Cai, Fang, Liu, Zheng, Zhu, Yong, Jin and Tang. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Fengfeng Cai
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