Elevated levels of phosphorylated cAMP response element binding protein is associated with lung tumorigenesis

RGS17, an overexpressed gene in human lung and prostate cancer, induces tumor cell proliferation through the cyclic AMP-PKA-CREB pathway.

CREB is overexpressed and constitutively phosphorylated in a number of forms of human cancer, including acute myeloid leukemia and non-small cell lung cancer, and appears to play a direct role in disease pathogenesis and prognosis.

ICAM-3 enhances the migratory and invasive potential of human non-small cell lung cancer cells by inducing MMP-2 and MMP-9 via Akt and CREB

demonstrated that GSK-3alpha is regulated by CREB in lung cancer and is required for the cell viability. These findings implicate CREB-GSK-3alpha axis as a novel therapeutic target for lung cancer treatment

Our results provide evidence that SETD2 and CREB1 contribute to cisplatin cytotoxicity in non-small cell lung cancer via regulation of the ERK signaling pathway, and their inactivation may lead to cisplatin resistance

This study demonstrates that the presence of rs928413(G) allele in the IL33 promoter results in its increased activity in a human lung carcinoma cell line due to binding of the cAMP (cyclic adenosine monophosphate) response element binding protein 1 (CREB1) transcription factor. The results offer a tentative explanation for the negative effect of rs928413 on asthma development.