results indicate that IAPs alone are not the main factor responsible for the resistance of non-small-cell lung cancer cells to treatment

XIAP protein has a role in preventing apoptosis in human lung cancer cells

These results suggest that XIAP polymorphisms do not significantly affect susceptibility to lung cancer in Koreans.

No relationship was found in serum XIAP and USP8 levels with clinical parameters, response to chemotherapy, and survival in patients with advanced stages of non-small cell lung cancer.

This paper highlights that targeting the BMP and TGFbeta type I and type II receptors causes a downregulation of XIAP, TAK1, and Id1 leading to cell death of lung cancer cells.

Study found a negative correlation between Smac and XIAP at the level of protein but not mRNA in non-small cell lung carcinoma (NSCLC) patients. Overexpressed XIAP could degrade through ubiquitination, the mature Smac inhibiting NSCLC apoptosis.

Inhibition of BET bromodomain-dependent XIAP and FLIP expression sensitizes KRAS-mutated non-small cell lung cancer to pro-apoptotic agents.

loss of XIAP enhances filopodia formation in a Cdc42-dependent manner and this phenomenon phenocopies EGF stimulation. Further, XIAP depletion promotes lung colonization of tumor cells in mice in a Cdc42-dependent manner. These observations shed molecular insights into ubiquitin-dependent regulation of Cdc42 and that of actin cytoskeleton.

MiR-142 inhibits lung cancer cell proliferation and promotes apoptosis by targeting XIAP.

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.

Combination of radiotherapy and inhibition of survivin and XIAP through the antisense approach results in improved tumor control by radiotherapy in a mouse model of lung cancer.