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Immune evasion in cancer: Mechanistic basis and therapeutic strategies.
Acquisition of epithelial-mesenchymal transition phenotype of gemcitabine-resistant pancreatic cancer cells is linked with activation of the notch signaling pathway.
TLDR
Molecular evidence is provided showing that the activation of Notch signaling is mechanistically linked with chemoresistance phenotype (EMT phenotype) of PC cells, suggesting that the inactivation of notch signaling by novel strategies could be a potential targeted therapeutic approach for overcoming chemores resistance toward the prevention of tumor progression and/or treatment of metastatic PC.
Metformin Inhibits Cell Proliferation, Migration and Invasion by Attenuating CSC Function Mediated by Deregulating miRNAs in Pancreatic Cancer Cells
TLDR
It is found that metformin significantly decreased cell survival, clonogenicity, wound-healing capacity, sphere-forming capacity (pancreatospheres), and increased disintegration of pancreatospheres in both gemcitabine-sensitive and gemcitABine-resistant pancreatic cancer cells.
Curcumin analogue CDF inhibits pancreatic tumor growth by switching on suppressor microRNAs and attenuating EZH2 expression.
TLDR
Results indicated that diflourinated-curcumin inhibited pancreatic cancer tumor growth and aggressiveness by targeting an EZH2-miRNA regulatory circuit for epigenetically controlled gene expression.
Exosomes in cancer development, metastasis, and drug resistance: a comprehensive review
TLDR
It is proposed that the successful combination of cancer treatments to tackle exosome-mediated drug resistance requires an interdisciplinary understanding of these cellular exclusion mechanisms, and how secreted biomolecules are involved in cellular cross-talk within the tumor microenvironment.
Over‐expression of FoxM1 leads to epithelial–mesenchymal transition and cancer stem cell phenotype in pancreatic cancer cells
TLDR
It is suggested, for the first time, that FoxM1 over‐expression is responsible for the acquisition of EMT and CSC phenotype, which is in part mediated through the regulation of miR‐200b and these processes, could be easily attenuated by genistein.
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