ShRNA‑mediated silencing of TARBP2 inhibits NCI‑H1299 non‑small cell lung cancer cell invasion and migration via the JNK/STAT3/AKT pathway.

Abstract

Metastasis is a major cause of lung cancer-associated mortality. The current study aimed to investigate the effects and mechanisms of TAR (human immunodeficiency virus1) RNA binding protein2 (TARBP2) in the invasion and migration of non‑small cell lung cancer invitro. The highly metastatic cell clone H1299/M02 was obtained by TARBP2 overexpression. Expression of TARBP2 in H1299/M02 was also downregulated to different levels via small hairpin RNAs (shRNAs). Subsequent to TARBP2 silencing, the proliferation of H1299/M02 cells was predominantly unaffected, while invasion and migration were significantly inhibited. A positive correlation was observed between invasion and migration and the level of TARBP2 silencing invitro. Western blotting and reverse transcription‑quantitative polymerase chain reaction indicated that the protein expression levels of amyloidβ(A4) precursor protein (APP) and zinc finger protein395 (ZNF395) were upregulated, while expression levels of pro‑metastatic proteins including interleukin (IL)‑1β, IL‑8, cyclooxygenase (COX)‑2, matrix metalloproteinase2 (MMP2) and MMP9 were downregulated. Phosphorylation of c‑Jun N‑terminal kinase (JNK), signal transducer and activator of transcription3 (STAT3) and protein kinaseB (AKT) were also inhibited. Overexpression of TARBP2 was suggested to be involved in the metastasis of H1299/M02 cells. Silencing of TARBP2 was able to upregulate levels of APP and ZNF395, in addition to inhibiting metastasis‑promoting cytokines, the JNK/STAT3/AKT pathway and COX‑2 to attenuate the invasion and migration of cancer cells.