Apoptosis induced by the combination of Apo2L/TRAIL and PG490 warrants evaluation as a treatment for lung cancer

The potentiation of TRAIL-induced cell death could be implicated in lung cancer therapy and prevention

Ioniing radiation signaling in a lung tumor cell line is due to release of TRAIL-associatted nuclear translocation of PAR-4 protein.

Data show that FHIT expression in lung cancer cells is protective from TRAIL-induced apoptosis, and that FHIT exerts this protective effect downstream of TRAIL-receptors and likely requires its dinucleoside-triphosphate hydrolase activity.

NF-kappaB targeting by way of IKK inhibition sensitizes lung cancer cells to adenovirus delivery of TRAIL

Epidermal growth factor receptor-mediated tissue transglutaminase overexpression couples acquired tumor necrosis factor-related apoptosis-inducing ligand resistance and migration through c-FLIP and MMP-9 proteins in lung cancer cells

AW00179 potentiates TRAIL-mediated cell death in the drug-resistant human lung cancer H1299 cells.

Oncolytic viruses selectively induced expression of TRAIL and Noxa in prostate cancer cells, lung cancer cells, and breast cancer cells downstream of RIG-I and MAVS.

Data indicate the importance of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) in pulmonary arterial hypertension (PAH) pathogenesis and suggest its potential as a therapeutic target to direct future translational therapies.

Increased serum S-TRAIL level in newly diagnosed stage-IV lung adenocarcinoma but not squamous cell carcinoma is correlated with age and smoking.

Overall survival in non-small cell lung cancer correlated with serum TRAIL levels.

Bcl-X(L) and p53-mediated amplification mechanisms played important roles in the sensitization of non-small-cell lung carcinoma cells to TRAIL-mediated apoptosis.

HUMSCs expressing ISZ-sTRAIL might be an efficient therapeutic approach against lung cancer and MCP-1/CCR2 axis is essential for the tumor tropism of HUMSCs

The nanovectorization of TRAIL enhanced its binding to both DR4 and DR5 receptors at 37 degrees C and could potentially sensitized cancer cells to TRAIL induced apoptosis through simultaneous activation of DR4 and DR5 as described in this paper for the non-small lung carcinoma cell line (H1703), the two hepatocarcinoma cell lines (SK-Hep1, HUH) and the colon carcinoma cell line (HCT116WT).

Apoptosis induced by TRAIL is preferentially induced by TRAIL-R1 pathway in breast/lung tumor cells.

Low soluble TRAIL level was associated with a shorter survival time of the non-small-cell lung carcinoma patients.

investigation of the gene polymorphisms in TRAIL molecular pathway and TRAIL gene expression levels in non-small cell lung cancer (NSCLC) patients in terms of pathogenesis and prognosis of the disease

tumor-suppressive activity of sTRAIL on circulating CD44+ cells in patients with non-small cell lung cancer.

Targeting bone morphogenetic protein receptor 2 sensitizes lung cancer cells to TRAIL by increasing cytosolic Smac/DIABLO and the downregulation of X-linked inhibitor of apoptosis protein.

CCR4NOT transcription complex subunit 2 regulates TRAIL sensitivity in nonsmallcell lung cancer cells via the STAT3 pathway.

Luteolin enhances TRAIL sensitivity in non-small cell lung cancer cells through increasing DR5 expression and Drp1-mediated mitochondrial fission.

Data indicate the importance of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) in pulmonary arterial hypertension (PAH) pathogenesis and suggest its potential as a therapeutic target to direct future translational therapies

tumor necrosis factor-related apoptosis-inducing ligand translates neonatal respiratory infection into chronic lung disease.