regulation of alternative splicing in lung adenocarcinoma cells by de novo ceramide

These results suggest a relevant role for STAT5 and Bcl-xL as apoptosis-regulatory proteins in the pathogenesis of lung cancer, and overexpression of both Neu and activated STAT3, could be related with the proliferation rate in lung carcinoma cells.

Bcl-XL siRNA contributes to an increase of cisplatin-induced cell death in non-small-cell lung cancer and sensitizes cells to cisplatin

non-small cell lung cancer cells were protected from apoptosis through increasing Bag3 expression and consequently promoted the expression of Bcl-XL and Bcl-2.

Bcl-xL silencing induces alterations in hsa-miR-608 expression and subsequent cell death in A549 and SK-LU1 human lung adenocarcinoma cells

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

CCAT1 is upregulated in docetaxel-resistant lung adenocarcinoma cells; its oncogenic function depends on sponging of let-7c, which releases Bcl-xl, promoting the acquisition of chemoresistance and epithelial-to-mesenchymal transition phenotypes