[Retracted] MicroRNA-375 inhibits glioma cell proliferation and migration by downregulating RWDD3 in vitro
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The authors of the above article drew to our attention that, in the above paper, 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 among the data panels, two pairs of panels in Fig. 4B were shown to be overlapping, and a further pair of panels showed overlapping data in Fig. 6B. The authors were presented with an opportunity to correct their figures in a Corrigendum, although it has subsequently come to light that the replacement figures themselves featured problems with overlapping data. Given the errors that have been identified in the compilation of the figures in this article, the Editor of Oncology Reports has decided that this article should be retracted from the publication owing to a lack of overall confidence in the presented data. The authors all agree to the retraction of this article, and the Editor and the authors apologize for any inconvenience that might result from this retraction. [the original article was published in Oncology Reports 39: 1825-1834, 2018; DOI: 10.3892/or.2018.6261].To study the effects of the miR-324-5p on the glioma cells proliferation via the targeted regulation of the glioma-associated oncogene 1.The luciferase reporter gene was used to test whether the glioma-associated oncogene 1 was the target of the miR-324-5p microRNA. The glioma-associated oncogene 1 expression was detected by Western blot. The proliferation and cell cycle were evaluated by MTT assay and flow cytometry.The glioma-associated oncogene 1 is a target of the miR-324-5p. An over-expressed miR-324-5p could reduce the cell survival rate and increase the G1/G0 phase rate in the glioma cell lines.The miR-324-5p can inhibit proliferation of the glioma cells via the targeted regulation of the glioma-associated oncogene 1.
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The expression of microRNA-203 (miR-203) in esophageal squamous cell carcinoma (ESCC) tissues is remarkably lower than that in non‑ESCC tissues. We investigated how miR-203 could influence the development of ESCC cells. Our analyses revealed that miR-203 inhibited the migration and invasion of ESCC cells. Genome-wide gene expression data and target site inhibition assays showed that miR-203 appears to directly regulate LIM and SH3 protein 1 (LASP1). The knockdown of LASP1 resulted in inhibition of the migration and invasion of ESCC cells. Our results suggest that miR-203 and its target LASP1, may be associated with the progression of ESCC. In clinical ESCC specimens, the expression levels of miR-203, which were lower compared to those in normal tissues, were inversely correlated with the mRNA expression levels of LASP1. Moreover, we found that there was a significant correlation between the expression levels of miR-203 and the relapse‑free survival. The identification of a cancer network regulated by miR-203 could provide new insights into the potential mechanisms of the progression of ESCC.
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Expression of RUNX3 gene and miR-363 in colorectal cancer was studied to explore its relationship with clinicopathological characteristics of colorectal cancer and to analyze the value of RUNX3 combined with miR-363 in the diagnosis of colorectal cancer. In total, 85 patients diagnosed with colorectal cancer in the First Peoples Hospital of Xiaoshan Hangzhou from March 2014 to July 2016 were the experiment group. Seventy healthy individuals who underwent physical examination were the control group. RT-qPCR was used to detect the expression levels of RUNX3 gene and miR-363 in peripheral blood of the two groups. The relationship between the expression of RUNX3 and miR-363 with its clinicopathological characteristics was analyzed as well. The expression of RUNX3 in the experiment group was significantly lower than that in the control group (P<0.05). The expression level of miR-363 was significantly lower than in the control group (P<0.05). However, there was a correlation with tumor size, degree of differentiation, lymph node metastasis, depth of invasion and clinical stages (P<0.05). RUNX3 and miR-363 were significantly positively correlated with the degree of differentiation (r=0.7381, r=0.5375; P<0.05); RUNX3 and miR-363 were significantly negatively correlated with clinical stages (r=-0.7167, -0.6700; P<0.05). The area under the ROC curve of the combined test was larger than the single test. The expression of RUNX3 gene and miR-363 in peripheral blood of patients with colorectal cancer was lower than in the normal controls. The low expression of RUNX3 and miR-363 was closely related to various biological behaviors of colorectal cancer. A potential reference is provided for the evaluation of patients with colorectal cancer and expected to have an important guiding effect in the treatment of colorectal cancer. Moreover, combined test of RUNX3 and miR-363 has important significance in the diagnosis and treatment evaluation of colorectal cancer.
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This study aimed to investigate FAM84B expression in glioma tissues and explore the role of FAM84B in promoting the proliferation of glioma cells and the mechanism of regulating the cell cycle pathways.The TCGA database was adopted to analyze FAM84B expression in glioma tissues. The FAM84B expression was detected by qRT-PCR in patients with glioma, especially that in glioma cells, U251, LN-229, U98, and U87. Two glioma cell lines U87 and T98 were selected for siRNA transfection, which were divided into si-NC si-FAM84B-1 and si-FAM84B-2 groups. The effect of FAM84B on the proliferation of glioma cells was detected with the MTT experiment and that on the glioma cell cycle was detected with the flow cytometry. The signaling pathways potentially regulated by FAM84B in glioma were analyzed through the bioinformatics analysis. The expression of proteins, Cyclin D1, CDK4, Cdk6, and p21, in the cell cycle-related pathways in cells of each group was detected by the Western blot.TCGA database results showed a significantly higher FAM84B expression in glioma tissues than that in paracancerous tissues. According to the detection of qRT-PCR, FAM84B expressed the highest in the glioma cell line U87 (P < 0.05). Compared with the serum of healthy controls, FAM84B mRNA expression significantly increased in patients with gliomas. And compared with the si-NC group, the proliferation ability of U87 and T98 cells decreased and the cell cycle was blocked in the G0/G1 phase in both si-FAM84B transfection groups (P < 0.05). According to the bioinformatics analysis, FAM84B regulated the cell cycle pathways in glioma. FAM84B siRNA inhibited the expression of key proteins, Cyclin D1, CDK2, CDK4, and Cdk6, of the cell cycle pathways in glioma cells and promoted the expression of P53 and P21 proteins.In conclusion, FAM84B may inhibit the proliferation of glioma cells by regulating the cell cycle pathways.
Cyclin-dependent kinase 6
U87
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Beclin 1 is involved in autophagy, differentiation, apoptosis and cancer progression, and functions as a haploinsufficient tumor suppressor gene. The aim of the present study was to elucidate the function of Beclin 1 in colon cancer. A Beclin 1-expressing plasmid was transfected into HCT-15 and HCT-116 cells, and the phenotypes and associated molecules were determined. Beclin 1 transfectants were subcutaneously injected into nude mice to determine tumor growth, and proliferation and apoptosis levels using Ki-67 immunostaining and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL), respectively. Beclin 1 overexpression inhibited viability as determined using a Cell Counting Kit-8 assay, inhibited migration and invasion as determined using a wound healing assay or Transwell assay, and lamellipodia formation by filamentous actin staining, induced autophagy as determined using electron microscopy, and light chain 3B (LC-3B) expression, and apoptosis as determined using Annexin V staining in the two cell lines (P<0.05). Beclin 1 induced G2 arrest of HCT-15 transfectants as determined using propidium iodide staining (P<0.05), whereas HCT-116 transfectants were arrested in G1 phase (P<0.05). The two transfectants exhibited increased expression of c-Myc, cyclin D1, β-catenin, insulin-response element 1 and 78 kDa glucose-regulated protein compared with the control and mock cells as determined using the reverse transcription-quantitative polymerase chain reaction (P<0.05). Beclin 1 overexpression upregulated LC-3B and cyclin-dependent kinase 4 expression, but downregulated cyclin E expression of the cancer cell lines as determined using western blot analysis (P<0.05). Beclin 1 expression in vivo significantly suppressed the proliferation of colon cancer cells in xenograft models via inducing apoptosis by TUNEL, and inhibiting proliferation by Ki-67 expression (P<0.05). Beclin 1 overexpression may reverse aggressive phenotypes and suppress colon cancer tumor growth, and be employed as a target molecule for gene therapy of patients with colon cancer.
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Long noncoding RNAs have been reported to be dysregulated and have pivotal roles in various human malignancies, including glioma. Previous studies revealed that metallothionein 1J (MT1JP) has important regulatory functions in the development of gastric cancer. However, the biological role and potential mechanism of MT1JP in glioma remain unknown. The present study suggested that MT1JP expression was significantly downregulated in glioma tissues and glioma cell lines, and the decreased expression of MT1JP was associated with glioma progression and poor survival of patients with glioma. Additionally, overexpression of MT1JP significantly inhibited the proliferation and invasion of glioma cells. Furthermore, it was revealed that MT1JP interacted with microRNA-24 (miR-24), which has previously been reported as an oncogene in glioma, negatively regulating its expression level. Rescue experiments revealed that the tumor suppressive functions of MT1JP may be mediated by the negative regulation of miR-24. Collectively, the data suggested that MT1JP inhibited the progression of glioma by negatively regulating miR-24 and may serve as a novel diagnostic biomarker and therapeutic target for glioma.
Tumor progression
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The invasiveness of glioma cells is the predominant clinical problem associated with this tumor type, and is correlated with pathological malignant grade. ZEB1 is highly expressed in glioma cells and associated with the aggressiveness of various types of cancer. In the present study, the expression of ZEB1 and ZEB2 was examined with the aim of determining the role of ZEBs in glioma. ZEB1 and ZEB2 were highly expressed in all glioma cells used in this study. Double knockdown of ZEB1 and ZEB2 suppressed tumor invasiveness more effectively than knockdown of either alone, in both in vitro and in vivo experiments. ZEB1 and ZEB2 were marginally expressed in grade II, but expressed at higher levels in grade IV. Importantly, ZEB-positive cells were more abundant in recurrent glioma with malignant transformation than in initial grade II tissue from the same case. These results indicate that the levels of ZEB1 and ZEB2 are positively correlated with histopathological grade and invasiveness of glioma, suggesting that δEF1 family proteins (ZEB1 and ZEB2) could be useful as prognostic markers and therapeutic targets in patients with glioma.
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Subsequently to the publication of the above article, the authors drew to the attention of the Editor that Figs. 5 and 6 both contained errors that arose inadvertently during the assembly of these figures. With the scratch wound assay data shown in Fig. 5A on p. 4043, the data panels showing the results from the '786‑O/NC' and '786‑O/miR‑216a inhibitor' experiments at t=0 h were overlapping, and similarly, the'786‑O/Migration, miR‑216a mimic' and '786‑O/Migration, NC' panels in Fig. 6A on p. 4044, showing the results of Transwell migration assay experiments, were overlapping, suggesting that these data were derived from the same original sources. After having consulted their original data, the authors realized where the errors occurred in assembling these figures, and were able to present the correct data for these figures to the Editorial Office. New versions of Figs. 5 and 6, showing the correct data for the '786‑O/miR‑216a inhibitor' experiment at t=0 h and the '786‑O/NC' experiment in Figs. 5A and 6A respectively) are shown on the next page. Note that the revised data shown for these figures do not affect the overall conclusions reported in the paper. All the authors agree with the publication of this corrigendum; furthermore, they apologize to the Editor of Experimental and Therapeutic Medicine and to the readership for any inconvenience caused. [Experimental and Therapeutic Medicine 15: 4039‑4046, 2018; DOI: 10.3892/etm.2018.5881]
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The purpose of the present study was to investigate the serum levels of microRNA (miRNA/miR)-382-3p, -598-3p, -1246 and -184 in breast cancer patients and to assess their feasibility as biomarkers for breast cancer screening. Serum samples were obtained from 100 breast cancer patients and 40 age-matched healthy control subjects in Taizhou Central Hospital (Taizhou, Zhejiang, China) between January 2013 and September 2014. The serum expression levels of miR-382-3p, -598-3p, -1246 and -184 were determined by stem-loop reverse transcription-quantitative polymerase chain reaction. Receiver operating characteristic curves were drawn to evaluate the sensitivity and specificity of the serum miRNA expression levels for the screening of breast cancer. miR-382-3p and -1246 were significantly upregulated in the serum of the breast cancer patients, while miR-598-3p and -184 were significantly downregulated. The sensitivity and specificity to detect breast cancer were as follows: miR-382-3p, 52.0 and 92.5%; miR-598-3p, 95.0 and 85.0%; miR-1246, 93.0 and 75.0%; and miR-184, 87.5 and 71.0%, respectively. The expression levels of the four serum miRNAs were not correlated with the patients' clinical stage. In summary, miR-382-3p, -598-3p, -1246 and -184 are all involved in the development of breast cancer, and are promising biomarkers for breast cancer detection.
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