1. Academic Validation
  2. Oroxylin A Suppresses the Cell Proliferation, Migration, and EMT via NF- κ B Signaling Pathway in Human Breast Cancer Cells

Oroxylin A Suppresses the Cell Proliferation, Migration, and EMT via NF- κ B Signaling Pathway in Human Breast Cancer Cells

  • Biomed Res Int. 2019 Jun 23:2019:9241769. doi: 10.1155/2019/9241769.
XiaoHu Sun 1 2 3 Xinzhong Chang 1 2 3 Yunhua Wang 4 Boyang Xu 4 Xuchen Cao 1 2 3
Affiliations

Affiliations

  • 1 Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Tianjin, China.
  • 2 Key Laboratory of Cancer Prevention and Therapy, Tianjin, China.
  • 3 Key Laboratory of Breast Cancer Prevention and Therapy, Tianjin Medical University, Ministry of Education, Tianjin, China.
  • 4 Tianjin University of Traditional Chinese Medicine, China.
Abstract

Oroxylin A is a natural extract and has been reported to have a remarkable Anticancer function. However, the mechanism of its Anticancer activity remains not quite clear. In this study, we examined the inhibiting effects of Oroxylin A on breast Cancer cell proliferation, migration, and epithelial-mesenchymal transition (EMT) and its possible molecular mechanism. The cytoactive and inflammatory factors were analyzed via Cell Counting Kit-8 assay and ELISA assay, respectively. Flow cytometry and western blotting were used to assess the cell proliferation. In addition, a wound healing assay and transwell assay were used to detect cell invasion and migration. qRT-PCR and western blot were employed to determine the effect of Oroxylin A on the EMT formation. Moreover, expression level of protein related to NF-κB signaling pathway was determined by western blot. The results revealed that Oroxylin A attenuated the cytoactivity of MDA-MB-231 cells in a dose- and a time-dependent manner. Moreover, cell proliferation, invasion, and migration of breast Cancer cells were inhibited by Oroxylin A compared to the control. The mRNA and protein expression levels of E-cadherin were remarkably increased while N-Cadherin and Vimentin remarkably decreased. Besides, Oroxylin A suppressed the expression of inflammatory factors and NF-κB activation. Furthermore, we also found that supplement of TNF-α reversed the effects of Oroxylin A on the cell proliferation, invasion, migration, and EMT in breast Cancer cells. Taken together, our results suggested that Oroxylin A inhibited the cell proliferation, invasion, migration, and EMT through inactivating NF-κB signaling pathway in human breast Cancer cells. These findings strongly suggest that Oroxylin A could be a therapeutic potential candidate for the treatment of breast Cancer.

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