epiregulin, COX2, and MMP1 and 2 collectively facilitate the assembly of new tumour blood vessels, the release of tumour cells into the circulation, and the breaching of lung capillaries by circulating tumour cells to seed pulmonary metastasis

Epiregulin expression correlates with advanced disease, is EGFR dependent, and confers invasive properties on non-small cell lung cancer cells.

Data indicate that epiregulin (EREG) expression significantly correlated with KRAS expression or KRAS copy number in KRAS-mutant non-small-cell lung cancer (NSCLC) cell lines.

we showed that epidermal growth factor receptors (EGFR) were constitutively activated in metastatic lung subtypes of salivary adenoid cystic carcinoma cells, and that this activation was induced by autocrine expression of epiregulin

The lack of the growth factor Ereg results in significantly reduced lung tumor development in a primary chemically induced tumor promotion model compared to wildtype controls (Ereg+/+ mice).

High expression of EREG is associated with lung carcinogenesis.