Analysis reveals that 5-fluorouracil nanoparticles reduce tumor growth in cervical cancer, implying NF-κB regulation's significance.
Background 5-Fluorouracil (5-FU) is a classic chemotherapy drug. Iron oxide nanocarriers (Fe 3 O 4 -NPs) significantly increase 5-FU concentration at tumor sites by enhancing targeting and sustained-release properties, while reducing systemic toxicity. Purpose Our research aims to explore the mechanism of the activity of novel 5-FU anti-tumor Fe 3 O 4 nanoparticles (NPs) in cervical cancer. Materials and Methods Prepare novel 5-FU-Fe 3 O 4 -NPs, analyze the nanomaterial properties through electron microscopy, the effect of 5-FU-Fe 3 O 4 -NPs on nuclear factor kappa B (NF-κB) expression was determined by reverse transcription polymerase chain reaction (RT-PCR), and cell proliferation was determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT). Flow cytometry and MTT detected cell biological behavior. 5-FU solution (control group) or 5-FU-Fe 3 O 4 -NPs were injected through the skin to treat skin metastases in nude mice, and the tumor volume was counted, and its size was measured. Results The average diameter of the NPs is 310 nm, and 70% of the particles are less than 385 nm, showing strong homogeneity. 5-FU-Fe 3 O 4 -NPs can inhibit NF-κB signaling molecule, a subunit of NF-κB transcription factor (P65) expression in cervical cancer cells, and the inhibition rate increases with the increase of 5-FU-Fe 3 O 4 -NPs concentration. 5-FU-Fe 3 O 4 -NPs can inhibit the increase in cervical cancer cell proliferation. Cell proliferation showed reduced surviving cells in 5-FU-NPs. Mouse cervical cell carcinoma also suggested that 5-FU-Fe 3 O 4 -NPs can significantly inhibit the growth of tumor cells, and this mechanism is mainly through inhibition of NF-κB expression. Conclusion 5-FU-Fe 3 O 4 -NPs, new anti-tumor NPs, can inhibit cell proliferation and promote apoptosis. 5-FU-Fe 3 O 4 -NPs, new anti-tumor NPs, can inhibit cell activities. It may slow down the proliferation of cervical cancer by regulating NF-κB signaling and have a significant anti-tumor effect.
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Zhang et al. (2025) studied this question.
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