Table 2.

FOXM1-mediated mechanisms of resistance to anti-metabolites.

SN	Cancer	Drug	FOXM1 role	Targets	Mechanisms of resistance	Ref
1	Colorectal cancer (CRC)	5-FU	Upregulated in nonresponsive CRC patients and 5-FU-resistant CRC cells. Overexpression evokes 5-FU resistance in CRC.	ABCC10	FoxM1-ABCC4 axis (ABCC10, a multidrug resistance (MDR) protein that actively efflux drugs from cells)	[157]
2	CRC	5-FU	Elevated FOXM1/TYMS expressions promote acquired 5-FU resistance in colon cancer cells (HCT116 5-FU Res). Pharmacological targeting of FOXM1 restored 5-FU sensitivity.	TYMS and other 5-FU targets	Partially through the regulation of TYMS. FOXM1 targets such as DDR genes, matrix metalloproteinases, and cell cycle regulators might also play a role in 5-FU resistance.	[48]
4	Esophageal cancer and CRC	5-FU	Up-regulation confers 5-FU resistance in CRC and esophageal cancer cells. Pharmacological targeting of FOXM1 restored 5-FU sensitivity.	-	FoxM1-dependent transcriptional activity and its downstream pathways.	[27, 50]
5	Gastric Cancer stem-like cells (CSCs)	5-FU	FoxM1 is required for redox homeostasis and survival of gastric CSCs against chemotherapeutics.	Prx3	FoxM1-dependent expression of Prx3 was strongly associated with low levels of ROS and 5-FU resistance.	[158]
6	AML	AraC	Overexpression is associated with reduced efficacy of AraC therapy. FOXM1 silencing enhances the sensitivity of AML cells to AraC.	-	FOXM1-dependent transcriptional activity.	[10, 51, 52]