Table 2.

Common KEGG pathways and leading-edge genes associated with COPD identified by GSEA (FDR_GSEA ≤ 0.25) in nasal and bronchial epithelium

	Nasal		Bronchial (cohort 1)		Bronchial (cohort 2)
	t-value	p value‡	t-value	FDR p value	t-value	p value‡
Enriched pathways for genes upregulated in COPD
O-glycan biosynthesis (KEGG)		0.01#		<0.01#		0.02#
GALNT6	3.00	<0.01	3.21	0.02	1.57	0.13
GALNT12	3.25	<0.01	3.32	0.01	3.83	<0.01
B3GNT6	2.51	0.02	3.55	<0.01	2.92	<0.01
ST6GALNAC1	2.65	0.01	3.44	<0.01	1.91	0.07
Glycosphingolipid biosynthesis (KEGG)a		0.04#		<0.01#		0.11#
FUT3	2.13	0.04	6.76	<0.01	2.68	0.01
FUT6	2.72	0.01	6.22	<0.01	2.77	0.01
B4GALT4	2.11	0.04	4.15	<0.01	0.12	0.90
B3GNT3	3.32	<0.01	5.06	<0.01	1.36	0.19
Enriched pathways for genes downregulated in COPD
DNA replication (KEGG)		<0.01#		0.09#		0.19#
RFC3	−2.36	0.02	−3.82	<0.01	−2.43	0.02
RNA degradation (KEGG)		<0.01#		0.06#		0.06#
Propanoate metabolism (KEGG)		0.13#		0.20#		0.09#
LDHB	−3.93	<0.01	−3.88	<0.01	−1.12	0.28
ACADM	−2.71	0.01	−6.06	<0.01	−2.14	0.04
ALDH3A2	−2.53	0.02	−4.57	<0.01	−1.15	0.26
Tight junction (KEGG)		0.13#		0.21#		0.24#
CLDN16	−2.33	0.02	−3.56	<0.01	−2.76	0.01
CTNNB1	−3.33	<0.01	−3.18	0.02	−1.65	0.11
EPB41L2	−2.64	0.01	−6.03	<0.01	−1.67	0.11

Above leading-edge genes of the 6 significantly enriched KEGG pathways in all three cohorts were significantly differentially expressed between COPD patients and controls both in nasal and bronchial epithelium (cohort 1). The t-value reflects the direction and the strength of the difference in expression of a gene between COPD and controls, FDR False discovery rate, ^#FDR_GSEA q value; ^‡nominal p-value. ^alacto and neolacto series