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Int J Mol Med. 2018 Oct;42(4):2221-2228. doi: 10.3892/ijmm.2018.3788. Epub 2018 Jul 19.

Melatonin inhibits epithelial‑to‑mesenchymal transition in gastric cancer cells via attenuation of IL‑1β/NF‑κB/MMP2/MMP9 signaling.

Author information

1
Central Laboratory, Fujian Medical University Union Hospital, Fuzhou, Fujian 350001, P.R. China.
2
Fujian Center for Safety Evaluation of New Drugs, Fujian Medical University, Fuzhou, Fujian 350108, P.R. China.

Abstract

Although melatonin has been shown to exert marked antitumor effects against a variety of cancers, the underlying mechanisms remain to be fully elucidated. It has been hypothesized that the anticancer properties of melatonin are associated with its ability to suppress epithelial‑to‑mesenchymal transition (EMT) of cancer cells. In the present study, melatonin effectively suppressed interleukin (IL)‑1β‑induced EMT in human gastric adenocarcinoma (GA) cells. Sequential treatment of GA cells with melatonin after IL‑1β challenge markedly reversed the IL‑1β‑induced morphological changes, reduced cell invasion and migration, increased β‑catenin and E‑cadherin expression, and downregulated fibronectin, vimentin, Snail, matrix metalloproteinase (MMP)2 and MMP9 expression. Moreover, IL‑1β‑induced activation of NF‑κB was attenuated following treatment with melatonin. Knockdown of NF‑κB significantly reduced the IL‑1β‑induced EMT in GA cells. Taken together, these findings indicate that melatonin may act by suppressing EMT and tumor progression by inhibiting NF‑κB activity.

PMID:
30066836
DOI:
10.3892/ijmm.2018.3788
[Indexed for MEDLINE]

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