Long non‑coding RNA BANCR mediates esophageal squamous cell carcinoma progression by regulating the IGF1R/Raf/MEK/ERK pathway via miR‑338‑3p

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‑diphenyltetrazolium 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.