Emerging role of the β-catenin-PPARγ axis in the pathogenesis of colorectal cancer

Table 1 Natural and synthetic compounds targeting Wnt/β-catenin and PPARγ pathways

	Subcategory	Drug	Pathways	Effects	Target tissues	Ref.
Natural ligands	Polyphenols	Quercetin EGCG Curcumin Resveratrol DIF	β-catenin/TCF WNT GSK-3β	β-catenin, TCF, cMyc, cyclin D1, survivin, conductin reduction	CRC, Adipose Tissue, Kidney	[81,91-101]
	Phytochemicals	Capsaicin Cladosporol Thymoquinone	β-catenin GSK-3β	β-catenin, cMyc reduction; GSK-3β, PPARγ activation	CRC	[89,102-105]
	Vitamins	Retinoids 1α25,-dihydroxy Vitamin D3	β-catenin Dab2	β-catenin reduction	CRC	[79,106-108]
Synthetic ligands	NSAIDs	Aspirin Sulindac Celecoxib Indometacin Diclofenac NS398	β-catenin, TCF, PPARγ	β-catenin, TCF cMyc reduction; PPARγ activation	CRC	[72-74,76,77,109-116]
	Small Molecules	PNU 74654 2,4-diamino-quinazoline ICG-001 FH535 Others	β-catenin/TCF CBP Dv1 Axin Tankyrase 1,2	Block Wnt Wnt/β-catenin suppression	CRC	[71-80]
	PPARγ ligands	TZDs Lutein	β-catenin/TCF	β-catenin degradation; PPARγ activation	CRC	[82-86,89]
	Partial PPARγ Agonists	Drug1	β-catenin/TCF	β-catenin degradation; PPARγ activation	CRC	[86-90]

NSAIDs: Non-steroidal anti-inflammatory drugs; CRC: Colorectal cancer.