Role of epithelial-mesenchymal transition in chemoresistance in pancreatic ductal adenocarcinoma

Table 1 Involvement of diverse miRNAs associated with epithelial-mesenchymal transition-mediated resistance in pancreatic ductal adenocarcinoma

miRNA	Signaling axis	Function	Ref.
miR-200	MiR-200/ZEB1/EMT	MiR-200 inhibited EMT and increased the sensitivity of GR PC cells to gemcitabine	[34]
miR-141	MiR-141/TM4SF1/AKT/EMT	MiR-141 inhibited EMT and reduced TM4SF1 expression by suppressing AKT signaling pathway	[35]
miR-203	MiR203-ZEB1-EMT	MiR-203 inhibited EMT and increased the sensitivity to gemcitabine	[43]
miR-223	MiR-223/Fbw7/Notch-1/EMT	MiR-223 induced EMT and conferred gemcitabine-resistance by downregulation of Fbw7 and subsequent upregulation of Notch-1	[45]
miR-331-3p	miR-331-3p/ST7L/Wnt/β-catenin/EMT	MiR-331-3p induced EMT and conferred gemcitabine-resistance by activating the Wnt/β-catenin signaling pathway via ST7L	[49]
miR-21	miR-21/PTEN/Akt	MiR-21 induced invasion, and metastasis, and conferred gemcitabine-resistance by miR-21/PTEN/Akt	[56]
miR-125a-3p	miR-125a-3p/Fyn/EMT	MiR-125a-3p inhibited EMT and increased chemosensitivity to gemcitabine by directly targeting Fyn	[57]
miR-145	miR-145/ ZEB1/EMT	MiR-145 inhibited EMT and reversed acquired gemcitabine resistance	[62]

EMT: Epithelial-mesenchymal transition; ZEB1: E-box binding homeobox 1; GR: Gemcitabine-resistant; PC: Pancreatic cancer.