Authors
Natalia Kurowska, Celina Kruszniewska-Rajs, Barbara Strzałka-Mrozik
Published in
Frontiers in molecular biosciences. Volume 13. Pages 1864680. Epub Jun 24, 2026.
Abstract
Colorectal cancer remains a leading cause of cancer-related mortality, with resistance to 5-fluorouracil (5-FU) posing a major therapeutic challenge. Thymoquinone (TQ), a bioactive compound derived from Nigella sativa, exhibits anticancer activity; however, its system-level effects in colorectal cancer are not fully understood.
RKO colorectal cancer cells were treated with TQ, 5-FU, or their combination for 24 h, followed by genome-wide transcriptomic profiling using oligonucleotide microarrays. Drug interaction effects were assessed using a deviation-from-additivity model. Selected genes were validated by RT-qPCR and Western blotting, and functional relevance was evaluated using bioinformatics analyses.
Combined treatment induced extensive network-level reprogramming of pathways associated with apoptosis, cellular stress response, and proliferation. Although no classical transcriptional synergy was observed, the interaction between TQ and 5-FU resulted in coordinated modulation of overlapping signaling networks. Key regulatory genes, including FAS and CYLD, were linked to enhanced pro-apoptotic signaling, whereas BIRC3 and EIF2AK3 were associated with adaptive or resistance-related responses.
TQ acts as a context-dependent modulator of chemotherapy response, reshaping cell death and stress-related signaling networks rather than directly enhancing cytotoxicity. These findings highlight the potential of TQ to influence therapeutic responses in fluoropyrimidine-based treatment of colorectal cancer and support further functional and in vivo validation.
PMID:
42422877
Bibliographic data and abstract were imported from PubMed on 09 Jul 2026.
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