PD-L1 gene expression in Japanese lung cancer patients

An imbalance in immune regulation affects tumor-specific T-cell immunity in the cancer microenvironment and reshapes tumor progression and metastasis. Blockade of interactions of immune function mediates antitumor activity in preclinical models. In the present study, we investigated programmed cell death 1 ligand 1 (PD-L1) mRNA expression by real-time polymerase chain reaction (RT-PCR) using a LightCycler in surgically treated non-small cell lung cancer (NSCLC) cases. This study included 123 surgically removed NSCLC cases for mRNA level analyses. The PD-L1/beta-actin mRNA levels showed no marked difference in lung cancer (131.398 +/- 421.596) and adjacent normal lung tissues (78.182 +/- 254092, P=0.1482). The tumor/normal (T/N) ratio of PD-L1/beta-actin mRNA levels was more than 2 in 49 cases and more than 1 in 63 cases. No difference was found in the T/N ratio of PD-L1/beta actin mRNA levels among factors inlcuding gender, age, smoking status and pathological subtypes. The T/N ratio of PD-L1/beta actin mRNA levels was markedly higher in pathological T4 cases (15.811 +/- 36.883) compared to T1 cases (3.492 +/- 8.494, P=0.0235). However, the PD-L1 mRNA status did not correlate with lymph node metastasis status. Thus, PD-L1 may drive tumor invasion, while providing a candidate for blockade of its function as a strategy to antagonize the progression process in NSCLC.