Table 1.

Gene expression was comprehensively profiled in 67LR bright highly tumorigenic cancer cells and 67LR dim cells

Source	Identifier	Pathway	P	Genes up in 67LR bright	Genes down in 67LR bright
KEGG	4510	Focal adhesion	<10−5	ITGA6, ITGAV, CAV1, LAMB3, LAMC2, PGF, SPP1, CAV3, IGFIR, LAMA3	BIRC3
KEGG	4110	Cell cycle	<10−5	SFN, CDKNIC	CDC2
KEGG	4012	ErbB signaling pathway	.0009	NRG2, HBEGF, MYC	AREG
KEGG	4330	Notch signaling pathway	.0004	DLL1, MFNG
KEGG	4150	mTOR signaling pathway	.005	HIF1A, PGF, DDIT4
KEGG	4310	Wnt signaling pathway	.0045	MYC, NFATC1, WNT10A	PRKACB
GO	6979	Response to oxidative stress	.0013	APOE, SOD2, HMOX1, PRNP, KRT1	IDH1
GO	6916	Anti-apoptosis	<10−5	APOE, NOL3, NRG2, BNIP3, SOCS3, HMOX1, PRNP, CRYAB, IGF1R	BIRC3
GO	6281	DNA repair	<10−5	SOD2, FANCE
GO	1558	Cell growth	.002	IGFBP2, DLC	PRSS2, PLCE1, ING3

The table lists selected functional pathways that were significantly enriched (adjusted p < .05) among differentially expressed genes between 67LR bright and dim cells, along with selected genes in each pathway showing statistically significant (adjusted p < 0.001) differential expression. Genes are listed according to official symbols in descending order of statistical significance. We added Kremen2 to the Wnt pathway category, but this addition was not considered in statistical analysis.