[Corrigendum] miR‑216a‑5p acts as an oncogene in renal cell carcinoma
Peijie ChenJing QuanLü JinCanbin LinXu WeijieJinling XuXin GuanZebo ChenLiangchao NiShangqi YangYun ChenYongqing Lai
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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]AIM: To study the antitumor mechanism of tubeimoside I (TBMS1), and to investigate its effects on cell division cycle and cell death in HeLa cells. METHODS: Cell growth inhibition of TBMS1 was measured by MTT assay; the induction of cell cycle arrest and apoptosis by TBMS1 was determined by flow cytometry, light, fluorescence and electron microscopies, and gel electrophoresis of fragmented DNA. Western blotting was performed for detecting the apoptosis related genes. RESULTS: TBMS1 displayed strong growth inhibitory effect against HeLa cells with estimated IC 50 values of 35.7 , 23.6 , and 17.4 μmol·L -1 . HeLa cells underwent G 2/M arrest with exposure to TBMS1, and had typical morphologic and biochemical evidence of apoptosis. Western blot analysis of TBMS1 treated cells revealed downregulation of bcl 2, and overexpression of bax. CONCLUSION: TBMS1 induced cell cycle arrest and apoptosis may play an important role in antitumor effect of TBMS1, and TBMS1 induced apoptosis is closely related to downregulation of bcl 2 and overexpression of bax.
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Objective To study effect of Caulilide(±)-1 on apoptosis and cell cycle, and its involved mechanism. Methods The DNA break was examined by DNA ladder. The cell cycle and the expression of apoptosis associated proteins were analysed by flow cytometry western blot respectively. The results were determined by flow cytometry. Results Caulilide(±)-1 could induce the apoptosis of S180 treated-group , which the DNA of the cells presentedlad-der. In LLC treated-group , the expressions of apoptosis associated protein of Bcl-2 displayed significant down-regulation, and the P53 did not show changes; Caulilide(±)-1 had a specific effect on cell division cycle of the LLC exposed to Caulilide(±)-1 for 48h, increased the number of cells in G0/G1 phase. Consults Caulilide(±)-1 can induce apoptosis of S180 and LLC. Its molecular mechanism may relate to modulation of the apoptosis associated proteins expression, and may be attributed to increase the number of cells in phase G0/G1.
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The aim of this study was to explore the effect of a traditional Chinese medicine (Xiaochaihu Tang, XCHT) on the expression of matrix metalloproteinase-2 (MMP-2) and MMP-9 in rats with endometriosis (EMs). A total of 48 specific-pathogen-free (SPF) female Sprague-Dawley (SD) rats were randomly divided into control (n=8) and EMs (n=40) groups. The EMs model was established using a surgical procedure. At 21 days, the rats with EMs were screened and divided into four subgroups (n=8): the model control, low-dose (7.5 g/kg) XCHT-treated, high-dose (15 g/kg) XCHT-treated and gestrinone-treated (0.5 mg/kg) groups. Following 21 days of treatment, the rats were sacrificed. Reverse transcription-polymerase chain reaction (RT-PCR) and western blotting were used to examine the mRNA and protein levels of MMP-2 and MMP-9 in the endometrium. The expression levels of MMP-2 and MMP-9 were significantly increased in the rats with EMs compared with those in normal rats. Moreover, XCHT was able to significantly inhibit the expression of MMP-2 and MMP-9 compared with that in the model control group. In conclusion, XCHT was able to decrease the expression of MMP-2 and MMP-9 in the ectopic endometrium. The present results may provide a potential theoretical basis for the therapy of EMs.
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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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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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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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Mediator complex subunit 15 (MED15) is a coactivator involved in the regulated transcription of RNA polymerase II‑dependent genes and serves an oncogenic role in numerous types of cancer. However, the expression and function of MED15 in hepatocellular carcinoma (HCC) remain unknown. In the present study, the aim was to investigate the expression and clinical significance of MED15 in HCC. Reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR) and immunohistochemical analysis revealed that MED15 mRNA and protein levels were significantly upregulated in HCC tissues compared with those in the corresponding adjacent non‑tumor liver tissues. Furthermore, analyzing data from The Cancer Genome Atlas‑Liver Hepatocellular Carcinoma (TCGA‑LIHC) and GSE14520 datasets revealed a significant correlation between MED15 expression and the tumor size (P=0.033), Barcelona Clinic Liver Cancer stage (P=0.031), α‑fetoprotein levels (P=0.002) and metastasis risk (P=0.001). Furthermore, patients with high MED15 expression levels had a shorter survival time compared with those with low MED15 expression levels (P<0.05). Univariate and multivariate analyses further revealed that MED15 may be an independent prognostic factor for the overall survival of HCC patients (hazard ratio, 1.762; 95% confidence interval, 1.077‑2.882; P<0.05). In addition, MED15 expression was positively associated with hypoxia‑inducible factor 1α expression in the TCGA‑LIHC and GSE14520 datasets (P<0.01). In conclusion, the data reported in the present study indicated that MED15 is overexpressed in HCC and may represent a novel prognostic biomarker for patients with HCC.
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