nicotine-induced survival and chemoresistance of human lung cancer cells may occur in a novel mechanism involving activation of PI3K/AKT that directly phosphorylates and inactivates the proapoptotic function of Bax

activation of the c-Abl-PKCdelta-Rac1-p38 MAPK pathway in response to ionizing radiation signals conformational changes of Bak and Bax, resulting in mitochondrial activation-mediated apoptotic cell death in human non-small cell lung cancer cells

The expression of p53, Bcl-2 and Bax was altered in lung cancer tissue compared to histologically normal bronchial epithelium.

Low expression of Bax was significantly associated with male gender, squamous cell histology and low expression of galectin-3 in lung cancer.

Bax G(-248)A polymorphism is associated with lung cancer susceptibility in Chinese population.

Reduced Bax expression after exposure to cisplatin is not sufficient to induce cisplatin-resistance in small cell lung ccancer cells.

TAp73alpha represses caspase-2 enzymatic activity and by this means reduces caspase-2 induced Bax activation, loss of mitochondrial transmembrane potential and resulting apoptosis in small cell lung carcinoma cells.

The expression levels of GRP78 and Bax were related to the carcinogenesis, development and metastasis of non-small cell lung cancer.

Depletion of end-binding protein 1 (EB1) promotes apoptosis of human non-small-cell lung cancer cells via reactive oxygen species and Bax-mediated mitochondrial dysfunction.

MA-1 treatment induced regulation of Bcl-2 family proteins in A549 lung cancer cells.

miR-511 regulates the growth of radioresistant lung cancer cells by increasing BAX expression through TRIB2.

BAX nuclear localization was associated in vivo with the remodelling of lung parenchyma during development, tumorigenesis as well as fibrosis compared to control adult human lungs