The expression of cathepsin L in non-small cell lung cancer is not related to the patients' outcome at a statistically significant level.

Cathepsins K, L, and S activity are profiled in 10 mug human breast, lung, and cervical tumors.

in vivo functional evidence for overexpressed CTSL as a promoter of lung metastasis, whereas high CTSL levels are maintained during tumor progression due to stress-resistant mRNA translation.

CTSL may contribute to gefitinib resistance in non-small-cell lung cancer

the findings demonstrated that mutated K-ras promotes cathepsin L expression and plays a pivotal role in EMT of human lung cancer. The regulatory effect of IR-induced cathepsin L on lung cancer invasion and migration was partially attributed to the Cathepsin L /CUX1-mediated EMT signaling pathway