[Retracted] MicroRNA­101 inhibits the proliferation and invasion of bladder cancer cells via targeting c­FOS.

Following the publication of this paper, it was drawn to the Editors' attention by a concerned reader that certain of the Transwell cell migration assay data shown in Fig. 5A were strikingly similar to data appearing in different form in other articles by different authors. Owing to the fact that the contentious data in the above article had already been published elsewhere, or were already under consideration for publication, prior to its submission to Molecular Medicine Reports, the Editor has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive any reply. The Editor apologizes to the readership for any inconvenience caused. [the original article was published in Molecular Medicine Reports 14: 2651-2656, 2016; DOI: 10.3892/mmr.2016.5534].

MicroRNA-101 inhibits cell migration and invasion in bladder cancer via targeting FZD4.

Dysfunction of microRNAs (miRs) has been implicated in the development and progression of various human cancers. Our previous study demonstrated that miR-101 inhibited bladder cancer cell proliferation and invasion through inhibition of c-FOS expression. As an miR generally has many targets, other targets of miR-101 may also serve important roles in bladder cancer progression. Reverse transcription-quantitative polymerase chain reaction and western blot analyses were used to examine mRNA and protein expression, respectively. Wound healing and Transwell assays were conducted to study cell migration and invasion, respectively. The luciferase reporter gene assay was performed to verify one of the targets of miR-101. The data in the present study indicate that the expression of miR-101 is significantly reduced in bladder cancer tissues compared with that in adjacent non-tumour tissues. In addition, miR-101 expression is also downregulated in bladder cancer cell lines compared with that in normal bladder epithelial cells. Furthermore, low expression of miR-101 was significantly associated with tumour metastasis, advanced clinical stage, and poor prognosis in bladder cancer. Frizzled class receptor 4 (FZD4) was identified as a novel target of miR-101 in bladder cancer cells. The expression of FZD4 was significantly upregulated in bladder cancer tissues and cell lines. Both miR-101 overexpression and FZD4 inhibition caused a significant reduction of the migration and invasion of bladder cancer cells, whereas overexpression of FZD4 reversed the suppressive effects of miR-101 on bladder cancer cell migration and invasion. In conclusion, it was demonstrated that miR-101 downregulation is associated with bladder cancer progression and that miR-101 can inhibit bladder cancer cell migration and invasion via directly targeting FZD4. The present study expands the understanding of the molecular mechanisms underlying bladder cancer progression.

Extracellular Histone Promotes Prostate Cancer Migration and Epithelial-Mesenchymal Transition through NF-κB-Mediated Inflammatory Responses.

INTRODUCTION: This study aims to explore the relationship betweenextracellular histone and prostate cancer and its mechanism. METHODS: Migration of prostate cancer cells was detected by Transwell. Inflammatory factor expression was investigated by ELISA. Epithelial-mesenchymal transition and expression of NF-κB pathway-related proteins were investigated using Western blotting. RESULTS: Under the induction of extracellular histones, the migration rate of prostate cancer cells and the levels of IL-1ß, TNF-α, and IL-6 were notably enhanced. Then, expression of E-cadherin was significantly down-regulated, while levels of N-cadherin, vimentin, ß-catenin, Snail, p-p65 and p-IκBα were significantly up-regulated, which was reversed by PDTC (pyrrolidine dithiocarbamate). CONCLUSION: Extracellular histone significantly promotes the progression of prostate cancer cells via NF-κB pathway-mediated inflammatory responses, which may serve as a novel target for treating prostate cancer.

MicroRNA-101 inhibits the proliferation and invasion of bladder cancer cells via targeting c-FOS.

MicroRNAs (miRs) have important roles in the parthenogenesis of malignancies. While it has been suggested that deregulation of miR­101 is involved in bladder cancer, the underlying mechanisms have remained largely elusive. The present study aimed to investigate the roles of miR­101 in the regulation of bladder cancer cell proliferation and invasion. Reverse­transcription quantitative polymerase chain reaction analysis revealed that the expression of miR­101 was significantly reduced in the HT­1376, BIU87, T24 and 5637 several human bladder cancer cell lines compared to that in the SV­HUC­1 normal bladder epithelial cell line. Furthermore, a Targetscan search and a luciferase assay were used to identify c­FOS as a novel target of miR­101, and western blot analysis indicated that the protein expression of c­FOS was shown to be negatively regulated by miR­101 in bladder cancer T24 cells; however, c­FOS mRNA expression was not affected. In addition, plasmid­mediated overexpression of miR­101 and small hairpin RNA­mediated inhibition of c­FOS significantly inhibited the proliferation and invasive capacity of T24 cells, as indicated by an MTT and a Transwell assay, respectively. However, plasmid­mediated overexpression of c­FOS reversed the inhibitory effects of miR­101 overexpression on T24­cell proliferation and invasion. In conclusion, the present study demonstrated that miR­101 inhibits the proliferation and invasion of bladder cancer cells, at least partly via targeting c­FOS, suggesting that miR-101/c­FOS signaling may represent a potential therapeutic target for bladder cancer.