
| 10.3892/ol.2018.8349
http://scihub22266oqcxt.onion/10.3892/ol.2018.8349
 C5920466!5920466!29725474
free
free
free
|  
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Oncol+Lett 2018 ; 15 (5): 7837-45 Nephropedia Template TP
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Telocinobufagin inhibits the epithelial-mesenchymal transition of breast cancer cells through the phosphoinositide 3-kinase/protein kinase B/extracellular signal-regulated kinase/Snail signaling pathway #MMPMID29725474Gao Y; Shi L; Cao Z; Zhu X; Li F; Wang R; Xu J; Zhong J; Zhang B; Lu SOncol Lett 2018[May]; 15 (5): 7837-45 PMID29725474show ga
Telocinobufagin (TBG), an active ingredient of Venenumbufonis, exhibits an immunomodulatory activity. However, its antimetastatic activity in breast cancer remains unknown. The present study investigated whether TBG prevents breast cancer metastasis and evaluated its regulatory mechanism. TBG inhibited the migration and invasion of 4T1 breast cancer cells. Furthermore, TBG triggered the collapse of F-actin filaments in breast cancer. The epithelial-mesenchymal transition (EMT) markers, vimentin and fibronectin, were downregulated following TBG treatment. However, E-cadherin was upregulated following TBG treatment. Snail, a crucial transcriptional factor of EMT, was downregulated following TBG treatment. Signaling pathway markers, including phosphorylated protein kinase B (P-Akt), p-mechanistic target of rapamycin (mTOR) and p-extracellular signal-regulated kinase (ERK), were decreased following TBG treatment. The same results were obtained from in vivo experiments. In conclusion, in vitro and in vivo experiments reveal that TBG inhibited migration, invasion and EMT via the phosphoinositide 3-kinase (PI3K)/Akt/ERK/Snail signaling pathway in breast cancer.�
  
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