Impacts of Brucea Javanica Oil Emulsion Injection on EpithelialMesenchymal Transition of Pancreatic Cancer AsPC-1 Cells by Regulating JAK2/STAT3 Signaling Pathway
DING Yongping1, MIAO Huayuan1*, GUO Xiaohong1, WANG Jianhong2
The aim of this study was to investigate the impacts of Brucea javanica oil emulsion injection on EMT (epithelial-mesenchymal transition) of pancreatic cancer cells by regulating JAK2/STAT3 signaling pathway. AsPC-1 cells from pancreatic cancer were grouped into control group, low dose group, medium dose group, high dose group, and high dose+Colivelin (JAK2/STAT3 activator) group. Cell scratch test was applied to detect cell migration; Transwell experiment was applied to detect cell invasion; MTT and EdU were applied to detect cell proliferation; flow cytometry was applied to detect cell apoptosis rate; qRT-PCR was applied to detect the expression of JAK2 mRNA and STAT3 mRNA in cells; Western blot was applied to detect the expression levels of JAK2/STAT3 pathway, E-cadherin, N-cadherin, and Vimentin proteins in cells. Result display, compared with the control group, the cell viability and proliferation rate, scratch healing rate, the number of invasive cells, the expression of JAK2 mRNA, STAT3 mRNA, N-cadherin, Vimentin, p-JAK2/JAK2, p-STAT3/STAT3 proteins in the low, medium, and high dose Brucea javanica oil emulsion groups obviously reduced, the apoptosis rate and the expression of E-cadherin in cells obviously increased (P<0.05). Compared with the high-dose Brucea javanica oil emulsion group, the cell viability and proliferation rate, scratch healing rate, the number of invasive cells, thew expression of JAK2 mRNA, STAT3 mRNA, N-cadherin, Vimentin, p-JAK2/JAK2, p-STAT3/STAT3 proteins in the high-dose Brucea javanica oil emulsion+Colivelin group obviously increased, the apoptosis rate and the expression of E-cadherin in cells obviously decreased (P<0.05). The study concluded that Brucea javanica oil emulsion can reduce AsPC-1 cell proliferation, migration, invasion, and EMT, possibly by inhibiting the JAK2/STAT3 signaling pathway.
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