AhR overexpression up-regulates the expression of CYP1B1 in the early stage of lung adenocarcinoma

AHR polymorphisms and potential gene-smoking interaction may be involved in the etiology of lung cancer.

Aryl hydrocarbon receptor activation and overexpression is associated with upregulation of fibroblast growth factor-9 resulting in lung adenocarcinomas.

The Aryl Hydrocarbon Receptor Signaling is the primarily affected pathway by the E6/E7 oncoproteins expression and this pathway is also deregulated in human small cell lung cancer.

AhR, without exposure to a ligand, associates with RelA, which then positively modulates NFkappaB activity and then upregulates IL-6 expression in human lung cells; a new mechanism for lung tumorigenesis

our data demonstrated that AhR protected lung adenocarcinoma cells against cigarette sidestream smoke particulate-induced oxidative stress and promoted post-exposure clonogenicity

Nuclear translocation of AhR was associated with EGFR mutation, and conferred a poor prognosis for patients with lung squamous cell carcinoma

Suggest that the AHR proximal promoter GGGGCrepeat polymorphism may have consequences for AhR expression and lung carcinogenesis.

AhR affects the transforming growth factor-beta signaling pathway by inducing Smad4 degradation by the proteasome and suppressing tumor metastasis via epithelial to mesenchymal transition reduction in lung cancer cells.

A low AHR-expression level in human lung cancer tissues is significantly associated with its malignancy.Cytoplasmic, resting AHR protein acts as an epithelial-mesenchymal transition suppressor via a non-genomic pathway.

A high AhR protein level indicated an unfavorable prognosis for non-small cell lung cancer (NSCLC). Inhibition of AhR signaling sensitized resistant NSCLC cells to EGFR tyrosine kinase inhibitors. Results provide proof-of-principle insights into a novel resistance mechanism driven by AhR where AhR acts as a protein adaptor to recruit Src and Jak2 kinases, rescuing PI3K/Akt and MEK/Erk signaling.

These results suggest that D-Kyn increases lung cancer cells to metastasize by activating Ahr.

The current data indicated that elevated Notch1 induced higher IL-22 secretion by CD4(+) T cells in lung adenocarcinoma patients, and Notch-AhR-IL-22 axis took part in the pathogenesis of lung adenocarcinoma.

Aryl hydrocarbon receptor mediates Jak2/STAT3 signaling for non-small cell lung cancer stem cell maintenance.