The oncoprotein N‑Myc has a carcinogenic effect in numerous types of cancer, and it can cause castration resistance in prostate cancer (PCa), and leads to the development of small cell neuroendocrine cancer by regulating multiple target genes. Immunohistochemical staining, RT‑qPCR, western blotting, wound healing and CCK‑8 assays were used to detect the expression of N‑Myc and FSCN1 as well as AR and CgA at the human level and cell level. The immunohistochemical results revealed that the protein levels of N‑Myc proto‑oncogene protein (N‑Myc) and fascin (FSCN1) in PCa were significantly higher than that of hyperplastic tissues (P less then 0.05), and there was a weak correlation between them (P=0.002). In vitro, N‑Myc and FSCN1 were overexpressed in LNCaP and C4‑2 cell lines. The results revealed the promoting effect of N‑Myc and FSCN1 on malignant progression of PCa. In addition, the endogenous FSCN1 was knocked down in the C4‑2 cell line, and the results revealed that the silencing of FSCN1 enhanced the expression of N‑Myc and weakened the expression of the neuroendocrine marker CgA. Therefore, the present findings indicated that N‑Myc may promote the malignant process of PCa by regulating FSCN1 and FSCN1 may have a reverse regulatory effect on N‑Myc.Estrogen receptor (ER)‑negative breast tumors are associated with low survival rates, which is related to their ability to grow and metastasize into distal organs. The aryl hydrocarbon receptor (AhR), a ligand‑activated transcription factor that is involved in several biological processes, is a promising anti‑metastatic target. Luteolin, a non‑toxic naturally occurring plant flavonoid with diverse biological activities, has been demonstrated to be effective against certain types of cancer, and has also been described as a ligand of AhR. In the present study, various cancer cell lines were first investigated following treatment with luteolin, and luteolin exhibited the lowest IC50 in MDA‑MB‑231 cells. Then, the efficiency of luteolin in suppressing the metastasis of ER‑negative breast cancer in vitro was assessed. MDA‑MB‑231 cells were treated with luteolin in vitro. Subsequently, MTT assay and flow cytometry were used to detect cell viability, the cell cycle and apoptosis, and a Transwell assay was used to evcould have promising clinical applications.DEAD‑Box Helicase 46 (DDX46) is an ATP‑dependent RNA helicase that plays a central role in transcription splicing and ribosome assembly. However, the role of DDX46 in cutaneous squamous cell carcinoma (CSCC) remains to be elucidated. CIA1 price The aim of the present study was to investigate the role of DDX46 in CSCC by assessing DDX46 expression levels in CSCC tissues and cell lines. The effect of DDX46 silencing on CSCC cell proliferation, apoptosis and autophagy were also analyzed. It was demonstrated that DDX46 was significantly overexpressed in CSCC tissues and cells (P less then 0.05). Furthermore, it was found that DDX46 silencing could dramatically inhibit cell proliferation (P less then 0.05). Moreover, cell apoptosis and autophagy were activated in DDX46 silencing groups (P less then 0.05). Therefore, the present results suggested that DDX46 was overexpressed in CSCC and that DDX46 silencing can inhibit cell proliferation by inducing apoptosis and activating autophagy. Thus, DDX46 may serve as a novel potential therapeutic target for CSCC.The authors of the above article drew to our attention that they had identified three instances of data overlapping between data panels, suggesting that data purportedly showing results obtained under different experimental conditions had been derived from the same original source. Comparing between the two figures, two pairs of panels in Fig. 4B (the Mimics control and blank experiments for the U87 and U251 cell lines) were shown to be overlapping, and a further pair of panels showed overlapping data in Fig. 6B (the data panels for the miR‑375 mi + .pCDNA/RWDD3 and miR‑375 mi + .pCDNA experiments for the U87 cell line). The authors were able to re‑examine the original data files and retrieve the correct data panels. The errors in these figures arose through inadvertently assembling Figs. 4 and 6 incorrectly. The revised versions of Figs. 4 and 6, featuring the corrected data panels for the Mimics control and blank experiments for the U87 and U251 cell lines in Fig. 4B, and the correct data for the U87 cell line in Fig. 6B, are shown opposite and on the next page, respectively. Note that the corrections to the data shown in these Figures do not affect the overall conclusions reported in the paper. The authors are grateful to the Editor of Oncology Reports for allowing them the opportunity to publish this Corrigendum, and apologize to the readership for any inconvenience caused. [the original article was published in Oncology Reports 39 1825-1834, 2018; DOI 10.3892/or.2018.6261].Long non‑coding RNAs (lncRNAs) have been implicated in various human malignancies, but the molecular mechanism of lncRNA TINCR ubiquitin domain containing (TINCR) in bladder cancer remains unclear. The present study found that the expression of TINCR was significantly increased in bladder cancer tissues and cell lines, when compared with that in adjacent normal tissues and normal urinary tract epithelial cell line SV‑HUC‑1, respectively. Moreover, the high expression of TINCR was associated with tumor metastasis and advanced tumor, node, metastasis stage, as well as reduced overall survival rates of patients with bladder cancer. Further investigation revealed that microRNA (miR)‑7 was negatively mediated by TINCR in bladder cancer cells. Silencing of TINCR expression significantly increased miR‑7 expression and reduced bladder cancer cell proliferation, migration and invasion, while knockdown of miR‑7 expression reversed the inhibitory effects of TINCR downregulation on bladder cancer cells. mTOR was then identified as a target gene of miR‑7 in bladder cancer, and it was demonstrated that overexpression of mTOR reversed the inhibitory effects of miR‑7 on bladder cancer cells. In conclusion, this study suggests that TINCR/miR‑7/mTOR signaling may be a potential therapeutic target for bladder cancer.