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Following the publication of the above paper, an interested reader drew to the authors' attention that, in Fig. 2D, the si‑ITGB3/E‑cadherin image appeared to show an overlap with the Scr/MDA231+CCL18/N‑cadherin image from Fig. 4E in a paper published in 2013 that shared some of the same authors [Zhang B, Yin C, Li H, Shi L, Liu N, Sun Y, Lu S, Liu Y, Sun L, Li X et al Nir1 promotes invasion of breast cancer cells by binding to chemokine (C‑C motif) ligand 18 through the PI3K/Akt/GSK3β/Snail signalling pathway. Eur J Cancer 49 3900‑3913, 2013]. Furthermore, the si‑Scb/E‑cadherin panel, also featured in Fig. 4D, appeared to show an overlap with a Figure included in the following paper that also featured some of the same authors, published in 2011 [Li W, Liu C, Tang Y, Li H, Zhou F and Lv S Overexpression of Snail accelerates adriamycin induction of multidrug resistance in breast cancer cells. Asian Pac J Cancer Prev 12 2575‑2580, 2011]. The authors were able to re‑examine their raw data, and identified the data that should have correctly been used in Fig. 2D in the above paper. The revised version of Fig. 2 is therefore shown on the next page, featuring the correct data panels for the si‑Scb/E‑cadherin and the si‑ITGB3/E‑Cadherin experiments. Note that these errors did not have a significant impact on the results or the conclusions reported in this study. The authors are grateful to the Editor of International Journal of Oncology for granting them the opportunity to publish this Corrigendum, and all the authors agree to the publication of this Corrigendum. The authors sincerely apologize for the errors presented in this figure, and apologize to the readership for any inconvenience caused.[the original article was published in International Journal of Oncology 48 1155‑1164, 2016; DOI 10.3892/ijo.2016.3319].Following the publication of this paper, it was drawn to the authors' attention by an interested reader that the Transwell invasion assay images in Fig. 3A had been duplicated and re‑presented within the same Figure. Furthermore, the same data were strikingly similar, in spite of their different presentation, to data featured in Fig. 2A of an article appearing in Oncology Research [Gu J, Cui, C‑F, Yang, L, Wang L and Jiang X‑H Emodin inhibits colon cancer cell invasion and migration by suppressing epithelial‑mesenchymal transition via the Wnt/β‑catenin pathway. Oncol Res 27 193‑202, 2019]. Finally, some of the tumour images featured in Fig. 6A of the above paper were strikingly similar to those featured in several other publications. The Editor asked the authors for an explanation to account for the appearance of strikingly similar data in their paper independently, and they responded to request that the paper be retracted from International Journal of Oncology. All the authors agreed that the article should be retracted. The Editor apologizes to the readership for any inconvenience caused.[the original article was published in International Journal of Oncology 51 657‑667, 2017; DOI 10.3892/ijo.2017.4034].Epidermal growth factor receptor pathway substrate 8 (Eps8) was initially identified as the substrate for the kinase activity of EGFR, improving the responsiveness of EGF, which is involved in cell mitosis, differentiation and other physiological functions. Numerous studies over the last decade have demonstrated that Eps8 is overexpressed in most ubiquitous malignant tumours and subsequently binds with its receptor to activate multiple signalling pathways. Eps8 not only participates in the regulation of malignant phenotypes, such as tumour proliferation, invasion, metastasis and drug resistance, but is also related to the clinicopathological characteristics and prognosis of patients. Therefore, Eps8 is a potential tumour diagnosis and prognostic biomarker and even a therapeutic target. This review aimed to describe the structural characteristics, role and related molecular mechanism of Eps8 in malignant tumours. In addition, the prospect of Eps8 as a target for cancer therapy is examined.The immune landscape of head and neck squamous cell carcinoma in pretreated areas remains poorly documented. We aimed to assess the tumor microenvironment for biomarkers of antitumor immune responses in tumors in previously irradiated areas compared with de novo tumors. This retrospective monocentric study analyzed 100 paraffin‑embedded surgical samples of invasive head and neck squamous cell carcinoma (oral cavity, oropharynx, larynx, hypopharynx) from patients who underwent surgery between January 2010 and November 2017. We compared the immune microenvironment in 50 de novo tumors and 50 tumors recurring within irradiated areas. We used immunohistochemistry to assess p16 status, CD3+/CD8+ tumor‑infiltrating lymphocytes (TILs), and programmed death‑ligand 1 (PD‑L1) expression on tumor and immune cells in stromal and intratumoral components. CD3+ TIL counts were significantly lower in intratumoral and stromal components (P=0.003 and P=0.020, respectively) in the irradiated area cohort; there was no significant difference between CD8+ TIL counts in the two cohorts. The percentage of tumors with PD‑L1+ tumor cells (tumor proportion score ≥1%) was significantly lower within the irradiated area cohort than the de novo cohort (56.0% vs. 86.0%, P less then 0.001). There were also significantly fewer tumors with PD‑L1+ immune cells in the irradiated area cohort. Predominantly, tumors from the irradiated area cohort had microenvironments classified as 'adaptive immune resistance'. There was persistence of cytotoxic cells in tumors in the irradiated areas but lower PD‑L1 expression and CD3+ TIL counts than in the de novo tumors. This offers an initial hypothesis to explain why these lesions are less responsive to immunotherapy, even though they may still have antitumor capacities. Assessment of immune response biomarkers in patients treated with immunotherapy in randomized trials is required.Interleukin‑6 (IL‑6) is involved in various biological responses, including tumor progression, metastasis and chemoresistance. However, the role and molecular mechanism of IL‑6 in the treatment of sorafenib in liver cancer remain unclear. In the present study, through western blot analysis, Transwell assay, flow cytometric assay, ELISA analysis and immunohistochemistry it was revealed that sorafenib promoted metastasis and induced epithelial‑mesenchymal transition (EMT) in liver cancer cells in vitro and in vivo, and significantly increased IL‑6 expression. Endogenous or exogenous IL‑6 affected metastasis and EMT progression in liver cancer cells through Janus kinase 2/signal transducer and activator of transcription 3 (STAT3) signaling. Knocked out IL‑6 markedly attenuated the pro‑metastasis effect of sorafenib and increased the susceptibility of liver cancer cells to it. In conclusion, the present results indicated that IL‑6/STAT3 signaling may be a novel therapeutic strategy for liver cancer.Chemotherapy with low‑molecular weight compounds, despite elimination of cancer cells, entails adverse effects. To overcome this disadvantage, innovative drug delivery systems are being developed, including conjugation of macromolecular carriers with therapeutics, e.g. a nanoconjugate of hydroxyethyl starch and methotrexate (HES‑MTX). The purpose of the present study was to determine whether HES‑MTX, applied as a chemotherapeutic, is able to modulate the immune response and support the antitumor response generated by dendritic cells (DCs) used subsequently as immunotherapeutic vaccines. Therefore, MTX or HES‑MTX was administered, as sole treatment or combined with DC‑based vaccines, to MC38 colon carcinoma tumor‑bearing mice. Alterations in antitumor immune response were evaluated by multiparameter flow cytometry analyses and functional assays. The results demonstrated that the nanoconjugate possesses greater immunomodulatory potential than MTX as reflected by changes in the landscape of immune cells infiltrating the tumor and increased cytotoxicity of splenic lymphocytes. In contrast to MTX, therapy with HES‑MTX as sole treatment or combined with DC‑based vaccines, contributed to significant tumor growth inhibition. However, only treatment with HES‑MTX and DC‑based vaccines activated the systemic specific antitumor response. In conclusion, due to its immunomodulatory properties, the HES‑MTX nanoconjugate could become a potent anticancer agent used in both chemo‑ and chemoimmunotherapeutic treatment schemes.It is estimated that one‑half of patients with non‑small cell lung cancer (NSCLC) undergo radiotherapy worldwide. However, the outcome of radiotherapy alone is not always satisfactory. The aim of the present study was to evaluate the effects of radiotherapy on the malignancy of NSCLC cells. It was demonstrated that radiation therapy could increase the migration and invasion of NSCLC cells in vitro. Moreover, the upregulation of visfatin, a 52‑kDa adipokine, mediated radiation‑induced cell motility. A neutralizing antibody specific for visfatin blocked radiation‑induced cell migration. Radiation and visfatin induced the expression of Snail, a key molecule that regulates epithelial to mesenchymal transition in NSCLC cells. Furthermore, visfatin positively regulated the mRNA stability of Snail in NSCLC cells, but had no effect on its protein degradation. This may be explained by visfatin‑mediated downregulation of microRNA (miR)‑34a, which was shown to bind the 3' untranslated region of Snail mRNA to promote its decay. Collectively, these findings suggested that radiation could induce cell motility in NSCLC cells through visfatin/Snail signaling.An increasing number of studies have demonstrated that long non‑coding (lnc)RNAs are associated with tumor invasion, metastasis and the prognosis of patients with a variety of different tumors. However, the roles of lncRNA prostate androgen regulated transcript 1 (PART1) in esophageal squamous cell carcinoma (ESCC) remain unknown. In the present study, reverse transcription‑quantitative PCR was performed to investigate the levels of PART1, SRY‑box transcription factor 6 (SOX6) and miR‑18a‑5p in ESCC tissues and cells. The functions of PART1 in ESCC were demonstrated using Cell Counting Kit‑8 and Matrigel assays. Promoter activity and dual‑luciferase reporter assays, RNA immunoprecipitation and western blot analyses were also used to determine the potential mechanisms of PART1 in ESCC cell lines. It was found that PART1 and SOX6 were both downregulated in ESCC tissues and cells, and their low expression levels were associated with TNM stage, lymph node metastasis and poor prognosis in patients with ESCC. Forkhead box protein P2 (FOXP2) exhibited low expression level in ESCC tissues, and its expression was positively correlated with PART1 expression level in ESCC tissues. FOXP2 was found to bind to the promoter region of PART1 to regulate its expression in ESCC cells. Functionally, PART1 overexpression suppressed cell proliferation and invasion, whereas PART1 downregulation promoted cell proliferation and invasion in the ESCC cell lines. Mechanistically, PART1 functions as a competing endogenous (ce)RNA by sponging miR‑18a‑5p, resulting in the upregulation of the downstream target gene, SOX6, coupled with the inactivation of the β‑catenin/c‑myc signaling axis, to suppress ESCC cell proliferation and invasion. Selleckchem EGFR inhibitor In conclusion, data from the present study unveil a potential ceRNA regulatory pathway, in which PART1 affects SOX6 expression level by sponging miR‑18a‑5p, to ultimately suppress ESCC development and progression.