Table 1.

Examples of genes in the IL-17 F pathway epigenetically altered in COPD and their respective roles in cancer

Epigenetically disrupted in COPD	Roles in cancer	References
IL-1α	Tumor cell-derived IL-1α increases tumor immunogenicity Precursor IL-1α from necrotic tumor cells promotes inflammation	[155]
IL-1β	Polymorphisms associated with overall cancer risk	[156]
IL-10	Polymorphisms associated with overall cancer risk Induces IFN-γ-mediated CD8+ anti-tumor immunity Treg cell-derived IL-10 suppresses Th17 inflammation	[157–159]
CCL2	Promotes metastasis and angiogenesis Recruits monocytes and macrophages contributing to inflammation	[160, 161]
CXCL1	Promotes metastasis, angiogenesis and cell proliferation Induces constitutive NF-κB activation Facilitates tissue damage	[162, 163]
GM-CSF/G-CSF	Promotes angiogenesis G-CSF contributes to myeloid derived suppressor cell recruitment at tumor site	[164, 165]
LCN2	Induces epithelial-mesenchymal transition (EMT) and promotes metastasis Promotes cell survival through iron sequesteration	[166, 167]
HBD1	Disrupts cell membrane and activates caspases in tumor cells Frequently lost in cancers, including prostate and renal cancers Recruits immature dendritic cell and memory T cell	[168, 169]