RESUMO
Subsequently to the publication of the above article, an interested reader drew to the authors' attention that a pair of data panels featured between Figs. 4 and 7 contained overlapping data such that the data were derived from the same original source where they were intending to depict the results from experiments performed under different experimental conditions, and a pair of the data panels featured in Fig. 8 for the ßcatenin data also appeared to show overlapping data. The authors were able to reexamine their original data, and have identified the data that were intended to have been shown for these figure parts. The corrected versions of Fig. 4 (showing the correct data for the LVDJ1/migration experiment in Fig. 4A), Fig. 7 (showing the correct data for the LVDJ1 + XAV939/migration experiment) and Fig. 8 (showing the correct data for the LVsiRNADJ1 experiment) are shown on the subsequent pages. The authors confirm that these inadvertent errors did not have any major impact on the conclusions reported in their paper, are grateful to the Editor of International Journal of Oncology for allowing them the opportunity to publish this Corrigendum, and apologize to the readership for any inconvenience caused. [the original article was published in International Journal of Oncology 56: 11151128, 2020; DOI: 10.3892/ijo.2020.5005].
RESUMO
DJ1, an oncogene, has been reported to be an independent prognostic indicator of poor survival in patients with esophageal squamous cell carcinoma (ESCC). The aim of the present study was to investigate the role of DJ1 in tumor cell proliferation and invasion in ESCC and its underlying mechanisms. It was observed that the expression level of DJ1 was upregulated and positively associated with EMT biomarkers in 84 human ESCC tissue specimens. Overexpression and knockdown experiments demonstrated that DJ1 was involved in proliferation, migration, invasion and EMT in ECA109 cells in vitro and extensive peritoneal seeding in a peritoneal dissemination mice model. Furthermore, the present data revealed that DJ1 could activate the Wnt/ßcatenin signaling pathway, which mediates the EMT and metastasis in ESCC. In conclusions, DJ1 promoted proliferation, invasion, metastasis and the EMT in ESCC via activation of the Wnt/ßcatenin signal pathway. The present results suggested DJ1 could represent a promising therapeutic target for the prevention and treatment of ESCCrelated metastasis.