Activation of caspase-3 and cleavage of Rb are associated with p16-mediated apoptosis in human non-small cell lung cancer cells.

Clinical significance of caspase-3 expression in pathologic-stage I, nonsmall-cell lung cancer

caspase-3, -8, and -9 activity is enhanced by safrole oxidase in lung cancer cells

Single nucleotide polymorphisms in the Caspase-3 gene is associated with lung cancer

Modulation of effector caspase-3 cleavage determines response of breast and lung tumor cell lines to chemotherapy.

Induction of apoptosis in human lung carcinoma cells by the water extract of Panax notoginseng is associated with the activation of caspase-3 through downregulation of Akt.

Thermo-chemotherapy has a stronger inhibitory effect than chemotherapy alone in lung tumor cell growth, probably through induction of ROS production and subsequent inhibition of Akt pathway activation and Caspase pathway-induced cancer cell apoptosis.

Single Nucleotide Polymorphisms in CASP3 is asspciated with lung cancer.

Data suggest that pulmonary metastasis is corrected with levels of Geminin, cleaved caspase-3, CD44, E-cadherin, epidermal growth factor receptor, and CD204 in cancer cells within permeated lymphatic vessels.

Low expression of CASP3 is associated with non-small cell lung cancer.

These results highlight apoptosis-related CASP3 as an important gene in human carcinogenesis and further support the CASP3 polymorphisms confer to the lung cancer susceptibility.

Caspase-3 knockout attenuates radiation-induced tumor repopulation via impairing the ATM/p53/Cox-2/PGE2 pathway in non-small cell lung cancer.

Identification of Sca-1(+)Abcg1(+) bronchioalveolar epithelial cells as the origin of lung adenocarcinoma in Gprc5a-knockout mouse model through the interaction between lung progenitor AT2 and Lgr5 cells.