lncRNA-u50535 promotes the progression of lung cancer by activating CCL20/ERK signaling

Abstract

The ligand/receptor pair C-C motif chemokine ligand 20 (CCL20)/C-C motif chemokine receptor 6 (CCR6) is considered to be highly activated in lung cancer and significantly accelerates lung cancer progression through activation of ERK signaling. In addition, it has been shown that long non-coding RNA-u50535 (lncRNA-u50535) upregulates CCL20 expression and facilitates cancer progression in colorectal cancer (CRC). However, the effects of lncRNA-u50535 in lung cancer progression and whether lncRNA-u50535 regulates CCL20/CCR6/ERK signaling in lung cancer remain ill-defined. Therefore, the aim of the present study was to investigate the effects of lncRNA-u50535 on CCL20/CCR6/ERK signaling in lung cancer progression. The results demonstrated that lncRNA-u50535 expression was upregulated in lung cancer tissues and cell lines compared with normal tissues and cells. Knockdown of lncRNA-u50535 decreased lung cancer cell proliferation and migration, induced G0/G1 phase arrest and promoted cell apoptosis. Western blot and luciferase reporter gene assays demonstrated that lncRNA-u50535 overexpression increased the translation and transcription of CCL20. In addition, knockdown of lncRNA-u50535 decreased CCL20, CCR6 and p-ERK levels. The effects of lncRNA-u50535 on cell proliferation and cell apoptosis were weakened when CCL20 was silenced. Overall, the present study demonstrated that lncRNA-u50535 may function as an oncogene in lung cancer progression by regulating CCL20/ERK signaling.