Peroxiredoxin 1 (Prdx1) is an antioxidant and plays an important role in H2O2-mediated cell signaling. We previously found that the expression level of Prdx1 was elevated in esophagus squamous cell carcinoma (ESCC) tissue using a proteomics approach. Since overexpressed protein can induce an autoimmune response, to further examine whether serum from ESCC patients exhibits immunoreactivity against Prdx1, autoantibody responses to Prdx1 were evaluated by ELISA, western blotting and indirect immunofluorescence assay in sera from patients with ESCC and normal individuals. Immunohistochemical study with tissue array slides and western blot analysis with cancer cell lines were also performed to analyze the protein expression profiles of Prdx1 in ESCC tissues and cancer cell lines. The results demonstrated that the positive rate of autoantibody against Prdx1 in ESCC sera was 13.2% (9/68), whereas this rate was 0% (0/89) in normal individuals. Data also showed that expression of Prdx1 was significantly increased in ESCC tissues when compared to expression in paired adjacent normal tissues (P<0.05). The data indicate that Prdx1 may contribute to malignant transformation of the esophagus, and may be used as a biomarker in the immunodiagnosis of ESCC.

MicroRNA‑590 (miR‑590) has been revealed as a tumor suppressor, while low‑density lipoprotein receptor‑related protein 6 (LRP6) is considered to act as a tumor promoter. However, their roles and underlying molecular regulatory mechanisms in esophageal squamous cell carcinoma (ESCC) have yet to be fully elucidated. Therefore, the present study aimed to investigate these mechanisms. The expression levels of miR‑590 and LRP6 in human ESCC samples and cell lines were determined using reverse transcription‑quantitative PCR. Bioinformatics analysis was used to predict the relationship between miR‑590 and LRP6, and luciferase assay was performed to validate the relationship between these factors. Transwell assays were used to determine cell migration and invasion, while western blotting assays were used to detect the protein expression levels of LRP6, E‑cadherin, N‑cadherin and Vimentin. The present study demonstrated that miR‑590 was downregulated and LRP6 was upregulated in ESCC tissues and cell lines. Furthermore, it was found that miR‑590 overexpression and LRP6 knockdown inhibited cell migration, invasion and epithelial‑to‑mesenchymal transition (EMT) in ESCC cell lines. Additional mechanistic studies identified that LRP6 was a target of, and was inhibited by, miR‑590. Collectively, the present findings suggested that miR‑590 inhibited the invasion, migration and EMT of ESCC cells by mediating LRP6.