Toll样受体4（TLR4）基因促进腺癌细胞迁移。吗啡是TLR4的激动剂，对癌症发展有双重作用。吗啡在癌症进展中的促进或抑制作用存在争议。本研究旨在评估吗啡对人类MDA-MB-231乳腺癌细胞株中TLR4、髓系分化初级反应蛋白88依赖蛋白（ MyD88）和核因子κB（NF-κB）表达的影响。细胞在吗啡孵育24小时后，使用Boyden 室系统进行检测。通过定量实时聚合酶链反应（RT-PCR）评估TLR4、MyD88和NF-κB mRNA表达，使用ELISA试验测定白细胞介素-2β的浓度。根据结果，三个剂量的吗啡（0.25、1.25和0.025μM）增加了TLR4和NF-κB基因的表达，而MyD88的mRNA表达没有显著变化。此外，吗啡和脂多糖（LPS）处理显著降低了TLR4、MyD88和NF-κB的表达。然而，白细胞介素-2β浓度没有明显变化。这些发现确认了吗啡在体外对TRL4表达和MyD88信号通路的兴奋作用。 版权声明：© 2023 高级生物医学研究。

The Toll-like receptor 4 (TLR4) gene promotes migration in adenocarcinoma cells. Morphine is an agonist for TLR4 that has a dual role in cancer development. The promoter or inhibitor role of morphine in cancer progression remains controversial. This study aims to evaluate the effects of morphine on the TLR4, myeloid differentiation primary response protein 88-dependent (MyD88), and nuclear factor-kappa B (NF-κB) expressions in the human MDA-MB-231 breast cancer cell line.The cells were examined after 24 hours of incubation with morphine using the Boyden chamber system. TLR4, MyD88, and NF-κB mRNA expressions were assessed using quantitative real-time polymerase chain reaction (RT-PCR). The concentration of interleukin-2 beta was also measured using the ELISA assay.According to the findings, three doses of morphine (0.25, 1.25, and 0.025 μM) increased the expression of the TLR4 and NF-κB genes, whereas no significant change was observed in the mRNA expression of MyD88. Furthermore, treatment with morphine and lipopolysaccharide (LPS) significantly decreased the expression of TLR4, MyD88, and NF-κB. However, no significant change was observed in interleukin 2 beta concentration.These findings confirmed the excitatory effects of morphine on TRL4 expression and the MYD88 signaling pathway in vitro.Copyright: © 2023 Advanced Biomedical Research.