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.

PurposeThis study was undertaken to establish a rabbit esophageal tumor model for mimicking human esophageal squamous carcinoma (ESC) by endoscopic and surgical implantation of VX2 tumors.MethodsFragments of a VX2 tumour were endoscopically implanted in the submucosal layer of the thoracic esophagus of 32 New Zealand white rabbits, while 34 animals received surgical implantation into the muscular layer. Then, the animals were studied endoscopically and pathologically. The safety and efficiency of the two methods and the pathological features of the animal models were analyzed.ResultsBoth the endoscopic and the surgical method had a relatively high success rate of tumor implantation [93.7% (30/32) vs. 97.1% (33/34)] and tumor growth [86.7% (26/30) vs. 81.8% (27/33)], and the variation in the results was not statistically significant (P>0.05). Compared with those produced by the surgical method, the models produced by the endoscopic method had a higher rate of severe esophageal stricture [61.5% (16/26) vs. 29.6% (8/27)] and of intra-luminal tumor growth [73.1% (19/26) vs. 37.0% (10/27)], and had a lower rate of tumor invasion of adjacent organs [53.8% (14/26) vs. 81.5% (22/27)]; all of these results were statistically significant (P<0.05). However, the difference in the survival time and the rates of tumor regional/distant metastasis [38.5% (10/26) vs. 51.8% (14/27)] between the two methods were not statistically significant (P>0.05).ConclusionThe endoscopic and surgical methods are both safe and effective for establishment of VX2 tumors in the rabbit esophagus. The models produced by the two methods have different pathologic features mimicking that of human ESC. We recommend the models for studies on surgical procedures and minimally invasive treatments.

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