Table 1.

Summary of preclinical in vitro evaluations of cranberries or cranberry derived constituents as cancer inhibitors.

Target	Cell Line(s)	Cranberry Constituent	In Vitro Results [Reference(s)]
Breast	MCF-7	CE	↑ apoptosis [23]; ↑ G1 cell cycle arrest [23]
			↓ cell viability [23,24]
		CJE	↓ cell viability [25]
		C-PAC	↓ cell density [26]
		FG	↓ cell viability [27]
		Fr6	↓ cell viability [28]
		Q	↓ cell viability [27]
		UA	↓ cell density [29,30]; ↓ cell viability [27]
	MDA-MB-435*	CJE	↓ cell viability [25]
		Fr6	↑ apoptosis [28]; ↑ G2-M cell cycle arrest [28]
			↓ cell viability [28]
		UA	↓ cell density [29]
Cervix	ME180	C-PAC	↓ cell density [26]
		UA	↓ cell density [30]
Colon	Caco-2	CJE	↓ cell viability [25]
		TP	↓ lipid peroxidation [31]
			↓ pro-inflammatory markers TNFα and IL-6 [31]
	HT-29	ANTHO	↓ cell viability [32]
		CE	↓ cell viability [24,33]
			↓ pro-inflammatory marker COX-2 [34]
		C-PAC	↑ apoptosis [35]; ↓ cell density [26]
			↓ cell viability [36]
		CJE	↓ cell viability [32]
		Fr6	↓ cell viability [36]
		TP	↓ cell viability [32]
		UA	↑ apoptosis [35]; ↓ cell density [29,30]
			↓ cell viability [35]
	HCT116	CE	↓ cell viability [33]
		C-PAC	↑ apoptosis [35]; ↓ cell viability [35]
		UA	↑ apoptosis [35]; ↓ cell density [29]
			↓ cell viability [35]
	LS-513	ANTHO	↓ cell viability [32]
		CJE	↓ cell viability [32]
		TP	↓ cell viability [32]
	SW460	TP	↓ cell viability [33]
	SW620	TP	↓ cell viability [24]
		C-PAC	↓ cell proliferation [37]
Esophagus	CP-C	C-PAC	↓ total reactive oxygen species [38]
	JHEsoAD1	C-PAC	↑ autophagy in acid-sensitive cells, pro-death [39,40]
			↑ necrosis in acid-resistant cells [39]
			↑ G2-M cell cycle arrest [39]
			↑ total reactive oxygen species [38]
			↑ hydrogen peroxide levels [38]
			↓ cell viability [40,41]
			↓ PI3K/AKT/mTOR signaling [39]
	OE33	C-PAC	↑ autophagy in acid-sensitive cells [39]
			↑ low levels of apoptosis [39]↑ G2-M cell cycle arrest [39]
			↓ cell proliferation [39]
			↑ total reactive oxygen species [38]
			↓ PI3K/AKT/mTOR signaling [39]
	OE19	C-PAC	↑ necrosis in acid-resistant cells [39]
			↑ G2-M cell cycle arrest with significant S-phase delay [39]
			↑ total reactive oxygen species [38]
			↑ hydrogen peroxide levels [38]
			↓ PI3K/AKT/mTOR signaling [39]
			↓ cell viability [40,41]
Glioblastoma	SF295	UA	↓ cell density [29]
	U87	C-PAC	↑ apoptosis [36]; ↑ G1 cell cycle arrest [36]
			↓ cell viability [36]
		Fr6	↑ apoptosis [36]; ↑ G1 cell cycle arrest [36]
			↓ cell viability [28]
Leukemia	K562	C-PAC	↓ cell density [26]
	RPMI8226	UA	↓ cell density [29]
Liver	HepG2	CE	↑ reduced glutathione levels [22]
			↓ glutathione peroxidase activity [22]
			↓ lipid peroxidation [22]
			↓ reactive oxygen species [22]
		CJE	↑ reduced glutathione levels [22]
			↓ glutathione peroxidase activity [22]
			↓ lipid peroxidation [22]
			↓ reactive oxygen species [22]
		FG	↓ cell viability [27]
		Q	↓ cell viability [27]
		UA	↓ cell viability [27]
Lung	DMS114	Fr6	↓ cell viability [28]
	NCI-H322M	UA	↓ cell density [29]
	NCI-H460	C-PAC	↑ apoptosis [37,42]; ↑ G1 cell cycle arrest [37]
			↓ cell density [26]; ↓ cell viability [37]
			↓ cell proliferation [37]
		UA	↓ cell density [29,30]
Lymphoma	Rev-2-T-6	NDM	↓ cell viability [43]
			↓ extracellular matrix invasion [43]
Melanoma	M14	C-PAC	↓ cell density [26]
		UA	↓ cell density [30]
	SK-MEL5	Fr6	↓ cell viability [28]
Neuroblastoma	IMR-32	C-PAC	↓ cell viability [44]
	SH-Sy5Y	C-PAC	↓ cell viability [44]
	SK-N-SH	C-PAC	↓ cell viability [44]
	SMS-KCNR	C-PAC	↑ apoptosis [44]; ↑ G2-M cell cycle arrest [44]
			↑ reactive oxygen species [44]
			↓ PI3K/AKT/mTOR signaling [44]
			↓ cell viability [44,45]
Oral Cavity	CAL27	CE	↑ apoptosis [46]; ↓ cell adhesion [46]
			↓ cell density [46]; ↓ cell viability [24]
		TP	↓ cell viability [33]
	HSC2	CJE	↑ reduced glutathione levels [47]
			↓ cell viability [47]
	KB	CE	↓ cell viability [24]
		TP	↓ cell viability [33]
	SCC25	CE	↑ apoptosis [46]; ↓ cell adhesion [46]
			↓ cell density [46]
Ovary	OVCAR-8	C-PAC	↑ G2-M cell cycle arrest [48]; ↓ cell viability [48]
	SKOV-3	C-PAC	↑ apoptosis [48,49]; ↑ G2-M cell cycle arrest [48,49]
			↑ reactive oxygen species [49]
			↓ AKT signaling [49]
			↓ cell proliferation [45,49]
			↓ cell viability [45,48,49]
Prostate	22Rv1	CE	↓ cell viability [33]
		TP	↓ cell viability [33]
	DU-145	CE	↑ G1 cell cycle arrest [50]
			↓ cell viability [50,51]
		C-PAC	↑ apoptosis [51]
			↑ MAPK signaling [52]
			↓ cell viability [26,36,51,52]
			↓ matrix metalloprotease activity [52]
			↓ PI3K/AKT signaling [52]
		Fr6	↓ cell viability [28,36]
	LNCaP	CE	↓ cell viability [24]
	PC3	CJE	↑ G1 cell cycle arrest [25]
			↓ cell viability [25]
		C-PAC	↓ cell density [26]
		UA	↓ cell density [30]
	RWPE-1	CE	↓ cell viability [33]
		C-PAC	↓ cell viability [33]
		TP	↓ cell viability [33]
	RWPE-2	CE	↓ cell viability [33]
		C-PAC	↓ cell viability [33]
		TP	↓ cell viability [33]
Renal	RXF393	UA	↓ cell density [29]
	SN12C	UA	↓ cell density [29]
	TK-10	UA	↓ cell density [29]
Stomach	AGS	CJE	↓ cell viability [25]
	SGC-7901	CE	↑ apoptosis [53]
			↓ cell proliferation [53]
			↓ cell viability [53]

Cranberry derived constituents are abbreviated as follows: anthocyanins (ANTHO), organic-soluble cranberry extract (CE), cranberry juice extract (CJE), cranberry proanthocyanidin-rich fraction (C-PAC), flavonoid-rich fraction 6 (Fr6), flavonoid glycosides (FG), non-dialyzable material from cranberry juice concentrate (NDM), total polyphenolic fraction (TP), quercetin (Q) or ursolic acid fraction (UA). Additional abbreviations: Phosphoinositide 3-kinase (PI3K), Protein Kinase B (AKT), mechanistic Target of Rapamycin (mTOR), mitogen-activated protein kinase (MAPK). Note: MDA-MB-435* was misidentified as a breast cancer cell line, but is now confirmed to be of melanoma origin.