Long non-coding RNA bancr mediates esophageal squamous cell carcinoma progression by regulating the igf1r/raf/mek/erk pathway via mir-338-3p

Abstract

Esophageal squamous cell carcinoma (ESCC) is a type of digestive tract malignant tumor that severely threatens human health. The long non-coding RNA BRAF activated non-coding RNA (BANCR) and insulin-like growth factor 1 receptor (IGF1R) are associated with various types of cancer; however, it remains unclear whether BANCR can regulate IGF1R expression in EScc. In the present study, the expression levels of BANCR, IGF1R mRNA and microRNA-338-3p (miRNA/miR-338-3p) in EScc tissues or cells were detected by reverse transcription-quantitative polymerase chain reaction (RT-qPcR). The levels of IGF1R, E-cadherin, N-cadherin, Vimentin, p-Raf-1, p-MEK1/2 and p-ERK1/2 were measured by western blot analysis. The proliferation, migration and invasion of EScc cells were determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetra-zolium bromide (MTT) or Transwell assays. The relationship between miR-338-3p and BANcR or IGF1R was predicted using starBase2.0 and confirmed by dual-luciferase reporter assay. The role of BANcR in EScc in vivo was confirmed through a tumor xenograft assay. It was found that BANcR and IGF1R were upregulated, while miR-338-3p was downregulated in EScc tissues and cells. Both BANcR and IGF1R knockdown suppressed the proliferation, migration, invasion and epithelial-mesenchymal transition (EMT) of EScc cells. IGF1R enhancement reversed BANcR knockdown-mediated effects on the proliferation, migration, invasion and EMT of EScc cells. BANcR regulated the Raf/MEK/ERK pathway by regulating IGF1R expression. Notably, BANcR regulated IGF1R expression by sponging miR-338-3p. Moreover, BANcR silencing inhibited tumor growth in vivo. On the whole, the findings of the present study demonstrate that BANcR inhibition blocks EScc progression by inactivating the IGF1R/Raf/MEK/ERK pathway by sponging miR-338-3p.