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Delphinidin Suppresses PMA-Induced MMP-9 Expression by Blocking the NF-κB Activation Through MAPK Signaling Pathways in MCF-7 Human Breast Carcinoma Cells
- Im, Nam-Kyung, Jang, Won Jun, Jeong, Chul-Ho, Jeong, Gil-Saeng
- Journal of medicinal food 2014 v.17 no.8 pp. 855-861
- secretion, signal transduction, Western blotting, metastasis, genes, neoplasm cells, mitogen-activated protein kinase, atherosclerosis, cytokines, gene expression, gelatinase B, transcription factor NF-kappa B, humans, transcription (genetics), antioxidants, rheumatoid arthritis, protein synthesis, fruits, inflammation, reverse transcriptase polymerase chain reaction, delphinidin, vegetables, breast neoplasms
- Matrix metalloproteinase-9 (MMP-9) plays an important role in the invasion and metastasis of cancer cells. The synthesis and secretion of MMP-9 can be stimulated by a variety of stimuli, including cytokines and phorbol 12-myristate 13-acetate (PMA), during various pathological processes, such as tumor invasion, atherosclerosis, inflammation, and rheumatoid arthritis, whereas MMP-2 is usually expressed constitutively. Delphinidin, an anthocyanidin present in pigmented fruits and vegetables, possesses potent antioxidant, anti-inflammatory, and antiangiogenic properties. In this study, we investigated the antiproliferative and antiinvasive effects of delphinidin on PMA-induced MMP-9 expression in MCF-7 human breast carcinoma cells using zymography, western blotting, reverse transcription–polymerase chain reaction, and Matrigel invasion assay. Delphinidin significantly suppressed PMA-induced MMP-9 protein expression in MCF-7 human breast carcinoma cells, and it also inhibited the MMP-9 gene transcriptional activity by blocking the activation of NFkappaB (NF-κB) through MAPK signaling pathways. Moreover, the Matrigel invasion assay showed that delphinidin reduces PMA-induced cancer cell invasion. These results suggest that delphinidin is a potential antimetastatic agent that suppresses PMA-induced cancer cell invasion through the specific inhibition of NF-κB-dependent MMP-9 gene expression.