Disrupted circadian control promotes oncogenesis in breast cancer

TL;DR

Disrupted circadian genes contribute to breast cancer progression by affecting DNA replication and cell signaling pathways.

Contribution

This study identifies specific circadian and hub genes dysregulated in breast cancer and links them to oncogenic processes.

Findings

1,788 differentially expressed genes were identified, including those involved in DNA replication and PI3K-Akt signaling.

Core circadian genes BMAL1, CLOCK, and PER3 were disrupted in breast cancer cells.

Downregulated genes were associated with cell adhesion and apoptosis, suggesting impaired tumor suppression.

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.