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Effects of the Co-Administration of Morphine and Lipopolysaccharide on Toll-Like Receptor-4/Nuclear Factor Kappa Β Signaling Pathway of Mda-Mb-231 Breast Cancer Cells Publisher



Kafami M1 ; Vaseghi G2 ; Haghjooy Javanmard S2 ; Mahdavi M3 ; Dana N2 ; Esmalianafyouni N4 ; Gohari A5
Authors
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Authors Affiliations
  1. 1. Cellular and Molecular Research Center, Department of Physiology and Pharmacology, Faculty of Medicine, Sabzevar University of Medical Sciences, Sabzevar, Iran
  2. 2. Applied Physiology Research Center, Cardiovascular Research Institute, Isfahan University of Medical Sciences, Isfahan, Iran
  3. 3. Applied Physiology Research Center, Isfahan University of Medical Sciences, Isfahan, Iran
  4. 4. Applied Physiology Research Center, Cardiovascular Research Center, Isfahan University of Medical Sciences, Isfahan, Iran
  5. 5. Department of Biochemistry and Nutrition, Faculty of Medicine, Sabzevar University of Medical Sciences, Sabzevar, Iran

Source: Advanced Biomedical Research Published:2023


Abstract

Background: 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. Materials and Methods: 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. Results: 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. Conclusions: These findings confirmed the excitatory effects of morphine on TRL4 expression and the MYD88 signaling pathway in vitro. © 2023 Medknow. All rights reserved.