AuthorWrite something about yourself. No need to be fancy, just an overview. ArchivesCategories |
Back to Blog
Dustwind nuclear snail4/20/2023 ![]() Gemcitabine as a single agent has been used as first-line chemotherapy for almost three decades ( 3), but its benefits in terms of survival are limited. Despite numerous efforts, the treatment options for PDAC remain limited, and the treatment outcomes are poor. Pancreatic ductal adenocarcinoma (PDAC) accounts for 90% of all cases of pancreatic cancer ( 1) and is one of the most lethal types of cancer, with an overall 5-year survival rate of only 9% ( 2). The findings of the present study suggested that C150 is a novel EMT inhibitor that may be promising for inhibiting pancreatic cancer growth and metastasis. Furthermore, C150 enhanced protein degradation of Snail, an important EMT-promoting transcription factor, and decreased the expression of the mesenchymal marker N-cadherin, while it increased the expression of the epithelial markers zonula occludens-1 and claudin-1. In an orthotopic mouse model of pancreatic cancer, C150 significantly reduced tumor growth at the dose of 15 mg/kg by intraperitoneal injection three times per week. Moreover, C150 treatment decreased MMP-2 gene expression in PANC-1 cells and reduced MMP-2 activity in gelatin zymography assay. C150 significantly inhibited pancreatic cancer cell migration and invasion, as demonstrated by 3-dimensional cell invasion, wound healing and Boyden chamber Transwell migration-invasion assays. C150 inhibited cell proliferation in multiple pancreatic cancer cells with IC 50 values of 1-2.5 μM, while in an non-cancerous pancreatic epithelial cell line hTERT-HPNE the IC 50 value was >12.5 μM. The aim of the present study was to report on the inhibitory effect of the novel compound C150 on the EMT of pancreatic cancer cells. Therefore, targeting EMT may be beneficial for pancreatic cancer treatment. Pancreatic cancer cell epithelial-to-mesenchymal transition (EMT) is an important contributor to cell invasion and tumor progression. 4Higuchi Biosciences Center, University of Kansas, Lawrence, KS, United States.3Biotechnology Innovation and Optimization Center, University of Kansas, Lawrence, KS, United States.2Department of Cancer Biology, University of Kansas Medical Center, Kansas City, KS, United States. ![]() ![]() 1Department of Pharmacology, Toxicology and Therapeutics, University of Kansas Medical Center, Kansas City, KS, United States.Tao Wang 1, Ping Chen 1, Ruochen Dong 1, Scott Weir 2, Michael Baltezor 3, Frank J. ![]()
0 Comments
Read More
Leave a Reply. |