Knockdown of POLE2 expression suppresses lung adenocarcinoma cell malignant phenotypes in vitro

In the present study, we profiled β‑elemene‑regulated gene expression and investigated the effects of the silencing of the DNA polymerase epsilon 2, accessory subunit (POLE2) in lung cancer cells. Differently expressed genes were profiled in A549 cells incubated in the presence or absence of β‑elemene by Affymetrix Human Gene Expression Array. POLE2 shRNA was then constructed to knock down POLE2 expression. Cells were counted and phenotypes were assessed via CCK‑8, colony formation and caspase-3/-7 activity assays. PathScan antibody array analysis was used to identify shPOLE2‑regulated genes. The cDNA microarray identified a total of 721 differentially expressed genes in the A549 cells. Furthermore, knockdown of POLE2 expression inhibited A549 and NCI‑H1299 cell proliferation and apoptosis. The PathScan data indicated that expression levels of p‑Akt (phosphorylated‑protein kinase B, p‑AKT/p‑PKB), p‑Smad2 (phosphorylated mothers against decapentaplegic homolog 2), p‑p38 MAPK (phosphorylated mitogen‑activated protein kinases p38), p‑SAPK/JNK (phosphorylated c‑Jun N‑terminal protein kinase/stress activated protein kinase), cleaved caspase‑7, IκBα (nuclear factor of κ light polypeptide gene enhancer in B‑cell inhibitor, α), p‑Chk1 (phosphorylated checkpoint kinase 1), p‑IκBα, p‑eIF2α (phosphorylated eukayotic translational initiation factor 2α), p‑TAK1 (phosphorylated TGF‑B‑activated kinase 1), survivin and α‑tubulin were significantly lower in shPOLE2 cells than these levels in the shCtrl cells. The PathScan data indicated that the expression levels of p‑p53 (phosphorylated tumor protein 53) were significantly higher in the shPOLE2 cells than these levels in the shCtrl cells. β‑elemene can restrain human lung cancer A549 and NCI‑H1299 cell proliferation and apoptosis by suppressing POLE2 expression.