ArticleApoptosis : an international journal on programmed cell death2026
Nicotine suppresses ferroptosis in colon cancer cells via HMOX1/NF-κB pathway to reduce oxaliplatin sensitivity.
Article in Apoptosis : an international journal on programmed cell death, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- PUM2 inhibits ferroptosis and enhances oxaliplatin resistance in COAD via the NEDD4L/NRF2 axis.Translational oncology · 2026Article
- Advances in ferroptosis and cuproptosis: implications for spinal cord injury.Molecular biology reports · 2026Review
- Heat Stress in the Liver of Chicken: Insights from Keap1-Nrf2 Pathway Mediated Ferroptosis and Cuproptosis via the HO-1/FDX1/Gpx4 Axis.Veterinary sciences · 2026Article
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5 authors.
Funding
Abstract
Background As the primary active component in tobacco, nicotine is significantly associated with chemotherapy resistance in colon cancer. However, the molecular mechanisms through which nicotine contributes to chemotherapy resistance in colon cancer cells remain unclear. Methods The effects of nicotine on malignant phenotypes and chemosensitivity of colon cancer cells were investigated through CCK-8 assays, Transwell assays, apoptosis assays, wound healing assays, and colony formation assays. The role of ferroptosis in nicotine-mediated chemotherapy resistance was explored by measuring intracellular levels of reactive oxygen species, iron ions, and malondialdehyde. Through RNA sequencing, the key mechanism by which nicotine inhibits ferroptosis in colon cancer cells was identified and further validated through cell-based experiments. Additionally, a xenograft tumor model was used to assess the impact of nicotine on oxaliplatin efficacy and ferroptosis in transplanted tumors. Results In vitro experiments demonstrated that nicotine enhanced malignant phenotypes and reduced the sensitivity of colon cancer cells to oxaliplatin. Furthermore, nicotine attenuated the chemotherapeutic effects of oxaliplatin by inhibiting oxaliplatin-induced ferroptosis. Mechanistic studies revealed that nicotine reduces the sensitivity of colon cancer cells to oxaliplatin by inhibiting ferroptosis through modulation of the HMOX1/NF-κB signaling pathway. In vivo experiments confirmed that xenograft tumors in nicotine-treated mice exhibited a significantly diminished therapeutic response to oxaliplatin, along with downregulated expression of ferroptosis markers in tumor tissues. ConclusionsThis study elucidates that nicotine suppresses ferroptosis in colon cancer cells via the HMOX1/NF-κB pathway to reduce oxaliplatin sensitivity. Targeted intervention of this pathway may offer a promising strategy to overcome nicotine-induced chemotherapy resistance.
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