Table 1.

EMT-mediated therapeutic resistance.

Tumor Types	Mechanisms	References
Breast	Inhibition of EMT and chemoresistance in breast cancer cells by miR-137.	[19]
Gastric	Cisplatin treatment of AGS and BGC-823 resulted in EMT. EMT enhances the ability of gastric cancer cells to migrate and invade	[61,95]
Cervical	TRIP4 depletion dramatically reduced cervical tumor cell proliferation and EMT	[71]
Colorectal	Snail, an EMT regulator, may induce chemoresistance by boosting the activity of the ABC transporter ABCB1. After exposure to ionizing radiation, rectal cancer cells displayed an EMT transition phenotype, which was reversed when miR-130a suppressed cell invasion.	[63,75]
Esophageal	miR-1275 specifically targeted WNT1, thereby inhibiting the Wnt/β-catenin signaling pathway in Esophageal cancer cells via EMT.	[76]
Glioblastoma	Inhibiting CXCL1 expression decreased the growth and radioresistance of Glioblastoma cells.	[72]
Nasopharyngeal	Increased EVI1 expression in Nasopharyngeal cells was related to a poor prognosis and was shown to cause chemo/radioresistance in these cells.	[73]
Liver	Overexpression of TNF-α and PD-L1 in Hepatocellular Carcinoma was related to a poor overall survival outcome.	[96]
Lung	HOXA-AS3 conferred resistance to cisplatin by downregulating homeobox A3 expression (HOXA3). Cisplatin resistance was also increased, as was the EMT induced by HOXA3 knockdown. Oct4/Nanog stimulation of the Wnt/β-catenin signaling pathway controls drug resistance and EMT changes. Inhibition of β-catenin abolished the multi-drug resistance and EMT processes mediated by Oct4/Nanog in lung cancer cells.	[60,83]