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Title

Disrupted circadian control promotes oncogenesis in breast cancer

 

Authors

Yasmin Fatima1, Mohammad Kashif2* & Prashant Ankur Jain1*

 

Affiliation

1Department of Computational Biology and Bioinformatics, Sam Higginbottom Institute of Agriculture, Technology and Sciences, Prayagraj, Uttar Pradesh, India; 2Department of Life Sciences, Parul Institute of Applied Sciences, Parul University, Vadodara, Gujarat, 391760, India; *Corresponding author

 

Email

Yasmin Fatima - E-mail: yasmin389@gmail.com
Mohammad Kashif - E-mail: kashifjmi.bioinfo@gmail.com, mohammad.kashif40858@paruluniversity.ac.in

Prashant Ankur Jain - E-mail: prashant.jain@shiats.edu.in

 

Article Type

Research Article

 

Date

Received November 15, 2025; Revised December 15, 2025; Accepted December 15, 2025, Published December 15, 2025

 

Abstract

Breast cancer progression is increasingly linked to disturbances in circadian rhythm genes, although the underlying molecular mechanisms remain poorly understood. Circadian rhythm genes help maintain normal biological processes and their disruption contributes to breast cancer development. Transcriptomic data from breast cancer (MCF-7) and normal breast (MCF-10A) cell lines from the GSE76370 dataset were analyzed using the limma R package to identify differentially expressed genes. Functional enrichment and network analyses using GO, KEGG, STRING and Cytoscape revealed 1,788 DEGs, including 1,008 upregulated genes involved in DNA replication, chromatin remodeling and PI3K-Akt signaling and 780 downregulated genes associated with cell adhesion and apoptosis. Disrupted expression of core circadian genes (BMAL1, CLOCK and PER3) and hub genes such as ACTB, GAPDH and CDK1 suggests that circadian gene dysregulation promotes breast cancer progression and represents a potential therapeutic target.

 

Keywords

Circadian rhythm, breast cancer, BMAL1, CLOCK, PER3, PI3K–Akt signalling, hub genes, transcriptomics, systems biology, network analysis.

 

Citation

Fatima et al. Bioinformation 21(12): 4945-4955 (2025)

 

Edited by

P Kangueane

 

ISSN

0973-2063

 

Publisher

Biomedical Informatics

 

License

This is an Open Access article which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. This is distributed under the terms of the Creative Commons Attribution License.