ArticleFrontiers in bioengineering and biotechnology2026
C1orf112 promotes breast cancer growth by modulating the cell cycle.
Article in Frontiers in bioengineering and biotechnology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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). Conclusion: C1orf112 contributes to breast cancer progression in association with cell cycle pathways, making it a potential diagnostic and therapeutic target with clinical applications.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.