Down-regulation of RAGE may be considered as a critical step in tissue reorganization and the formation of lung tumours.

Data suggest that re-expression of the receptor for advanced glycation end-products in lung cancer cells impairs the proliferative stimulus mediated by fibroblasts.

it is concluded that CDK5RAP3, CCNB2, and RAGE genes may be used as a very reliable biomarkers of lung adenocarcinoma

The results showed that RAGE and its splice variants increased in esophageal cancers and decreased in lung cancers.

association between genetic polymorphisms of RAGE and susceptibility, chemotherapy response rate and prognosis of non-small cell lung cancer (NSCLC); the 82SS genotype and 82S allele distribution not only increased the NSCLC risk, but also was associated with a lower chemotherapy response rate and poor prognosis

Potential interactive contribution of RAGE and APE1 genes to the pathogenesis of lung cancer.

The polymorphism of rs2070600 in the RAGE gene may increase the susceptibility to several human cancers, especially to lung cancer and to Asians. The rs1800264 most likely contributes to decreased susceptibility to breast cancer but increased susceptibility to lung cancer (Meta-Analysis)

In conclusion, these data indicated that common polymorphisms in the AGER gene might increase the risks of breast (BC) and lung (LC) cancer .

High RAGE expression is associated with lung cancer.

Taken together, these observations suggest that Long non-coding RNA AGER-1 has an inhibitory effect on lung cancer development via AGER, which may serve as a target for lung cancer treatment.

Low expression of AGER was specifically associated with poor survival in lung adenocarcinoma.

Effect of AGER on the biological behavior of nonsmall cell lung cancer H1299 cells.

Overexpression of the secretory receptor in lung cancer cell lines had an inhibitory effect on cell proliferation, suggesting the reduced receptor expression accelerated tumor growth.

RAGE is at least one of the critical receptors for CS and HS chains expressed at the tumor cell surface and involved in experimental lung metastasis and that CS/HS and RAGE are potential molecular targets in the treatment of pulmonary metastasis.