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Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that several of the panels showing the results from cell migration and invasion assay experiments in Fig. 2 on p. 628 contained sections of data that were overlapping with other panels within the same figure. Given the issue of the overlapping sections of data, the Editor of Molecular Medicine Reports has decided that this paper should be retracted from the Journal on account of an overall lack of confidence in the presented results. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a satisfactory reply. The Editor apologizes to the readership for any inconvenience caused. [Molecular Medicine Reports 8: 626630, 2013; DOI: 10.3892/mmr.2013.1501].
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[This retracts the article DOI: 10.3892/ol.2013.1123.].
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Following the publication of the above article, an interested reader drew to the authors' attention that the cell and invasion migration assay data featured in Figs. 2C and 5D contained two pairs of overlapping panels, such that the data appeared to have been derived from the same original sources, even though the data panels were intending to show the results from differently performed experiments. Moreover, there was also an instance of duplicated data panels comparing between the siNC/cell invasion and siNC/cell migration assay panels in Fig. 4C. After having examined their original data, the authors have realized that inadvertent errors were made during the process of compiling these figures. Corrected versions of Figs. 2, 4 and 5, incorporating all the data from one of the repeated experiments, are shown opposite and on the next page. The authors all agree to the publication of this corrigendum, and are grateful to the Editor of Oncology Reports for allowing them the opportunity to publish this. They also regret any inconvenience caused to the readership of the Journal. [Oncology Reports 57: 35023508, 2017; DOI: 10.3892/or.2017.5607].
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Subsequently to the publication of this paper, an interested reader drew to the authors' attention that, in Fig. 3 on p. 4382, the 'Invasion' assay data for the negative control (NC) experiments for the T24 and EJ cell lines appeared to contain an overlap of data, such that they may have been derived from the same original source even though the data were purportedly intended to show the results from differently peformed experiments. The authors have reexamined their original data, and realize that this figure was inadvertently assembled incorrectly. The revised version of Fig. 3, showing alternative data from one of the repeated experiments, is shown below. Note that this error did not significantly affect either the results or the conclusions reported in this paper, and all the authors agree to this corrigendum. Furthermore, the authors thank the Editor of Molecular Medicine Reports for allowing them the opportunity to publish this corrigendum, and apologize to the readership for any inconvenience caused. [Molecular Medicine Reports 13: 4379-4385, 2016; DOI: 10.3892/mmr.2016.5055].
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The long noncoding RNA nicotinamide nucleotide transhydrogenase antisense RNA 1 (NNT-AS1) is a key malignancy regulator in a variety of human cancers. In this study, we first measured the expression of NNT-AS1 in bladder cancer and examined its role in cancer progression. The mechanisms behind the oncogenic functions of NNT-AS1 in bladder cancer were explored. We found that NNT-AS1 was upregulated in bladder cancer tissues and cell lines. This increased expression demonstrated a significant correlation with advanced clinical stage, lymph node metastasis, and shorter overall survival. NNT-AS1 knockdown suppressed bladder cancer cell proliferation, migration, and invasion and facilitated apoptosis in vitro and hindered tumor growth in vivo. NNT-AS1 functioned as a competing endogenous RNA for microRNA-496 (miR-496), and the suppressive effects of NNT-AS1 knockdown on malignant characteristics were abrogated by miR-496 silencing. HMGB1 was identified as a direct target gene of miR-496 in bladder cancer, and HMGB1 expression was enhanced by NNT-AS1 via sponging of miR-496. In conclusion, the NNT-AS1-miR-496-HMGB1 pathway plays a significant role in the aggressive behavior of bladder cancer and may lead to new NNT-AS1-based diagnostics and therapeutics.
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Proteína HMGB1/metabolismo , MicroARNs/metabolismo , Neoplasias de la Vejiga Urinaria/metabolismo , Neoplasias de la Vejiga Urinaria/patología , Línea Celular Tumoral , Movimiento Celular , Proliferación Celular , Regulación hacia Abajo , Femenino , Regulación Neoplásica de la Expresión Génica , Técnicas de Silenciamiento del Gen , Proteína HMGB1/genética , Humanos , Masculino , MicroARNs/genética , Persona de Mediana Edad , ARN Largo no Codificante , Neoplasias de la Vejiga Urinaria/genéticaRESUMEN
The electroreduction of carbon dioxide (CO2 ) toward high-value fuels can reduce the carbon footprint and store intermittent renewable energy. The iodide-ion-assisted synthesis of porous copper (P-Cu) microspheres with a moderate coordination number of 7.7, which is beneficial for the selective electroreduction of CO2 into multicarbon (C2+ ) chemicals is reported. P-Cu delivers a C2+ Faradaic efficiency of 78 ± 1% at a potential of -1.1 V versus a reversible hydrogen electrode, which is 32% higher than that of the compact Cu counterpart and approaches the record (79%) reported in the same cell configuration. In addition, P-Cu shows good stability without performance loss throughout a continuous operation of 10 h.
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Introduction of lattice strain into catalysts is a facile way to modify catalytic behaviour. Here, we report the synthesis of Pd nanoparticles with compressive strain by pulsed laser ablation of a Pd target immersed in an aqueous solution. The intensive quenching effect induces obvious compressive strain which improves the ORR performance of the Pd nanoparticles significantly.
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Low-cost and high-performance catalysts are of great significance for electrochemical water splitting. Here, it is reported that a laser-synthesized catalyst, porous Co0.75 Ni0.25 (OH)2 nanosheets, is highly active for catalyzing overall water splitting. The porous nanosheets exhibit low overpotentials for hydrogen evolution reaction (95 mV@10 mA cm-2 ) and oxygen evolution reaction (235 mV@10 mA cm-2 ). As both anode and cathode catalysts, the porous nanosheets achieve a current density of 10 mA cm-2 at an external voltage of 1.56 V, which is much lower than that of commercial Ir/C-Pt/C couple (1.62 V). Experimental and theoretical investigations reveal that numerous Co3+ ions are generated on the pore wall of nanosheets, and the unique atomic structure around Co3+ ions leads to appropriate electronic structure and adsorption energy of intermediates, thus accelerating hydrogen and oxygen evolution.
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Unraveling a descriptor of catalytic reactivity is essential for fast screening catalysts for a given reaction. Transition metal (TM) compounds have been widely used for oxygen electrocatalysis. Nevertheless, there is a lack of an exact descriptor to predict their catalytic behavior so far. Herein, we propose that the bond-energy-integrated orbitalwise coordination number ([Formula: see text]), which takes into account both geometrical and electronic structures around the active site, can serve as a simple and accurate descriptor for catalysts consisting of TM oxides (TMOs) as well as avoid excessive computation burden. This descriptor exhibits a strong scaling relation with the activity in oxygen electrocatalysis, with a goodness of fit higher than those of the usual coordination number (cn), the generalized coordination number ([Formula: see text]), and the orbitalwise coordination number (CNα). Especially, the theoretical prediction made by the [Formula: see text] descriptor is very consistent with experimental results and universal for various TMOs (e.g., MnO x and RuO2), enabling the rational design of novel catalysts.
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Bladder cancer is the second most common urological malignancy in the US and is the most frequently diagnosed urological malignancy in China. An increasing amount of evidence indicates that microRNAs perform extremely important functions in many biological processes related to the formation and progression of cancers, including bladder cancer. Previous studies have reported that microRNA379-5p (miR-379-5p) is involved in tumour initiation and development in human cancers. However, the expression pattern, biological functions and the underlying mechanisms of miR-379-5p in bladder cancer remain unknown. The present study demonstrated that the expression levels of miR379-5p in bladder cancer tissues and cell lines were lower than the levels in adjacent normal tissues and the human bladder epithelial immortalized SV-HUC-1 cell line. Restoration of the expression of miR-379-5p inhibited bladder cancer cell proliferation, migration and invasion. Mouse double minute 2 (MDM2) was identified as a direct target gene of miR-379-5p. Furthermore, similar to miR-379-5p overexpression in bladder cancer cells, inhibition of MDM2 exerted tumor-suppressive effects. Rescue experiments showed that upregulation of MDM2 reversed the inhibitory effects of miR-379-5p on bladder cancer cell proliferation, migration and invasion. MDM2 was highly expressed and inversely correlated with miR-379-5p expression in bladder cancer tissues. These findings suggest that the miR-379-5p/MDM2 pathway plays an important role in bladder cancer and could serve as a potential candidate for bladder cancer therapeutics.
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Proliferación Celular/genética , MicroARNs/genética , Proteínas Proto-Oncogénicas c-mdm2/genética , Neoplasias de la Vejiga Urinaria/genética , Línea Celular Tumoral , Movimiento Celular/genética , Femenino , Regulación Neoplásica de la Expresión Génica , Humanos , Masculino , MicroARNs/antagonistas & inhibidores , Invasividad Neoplásica/genética , Metástasis de la Neoplasia , Proteínas Proto-Oncogénicas c-mdm2/antagonistas & inhibidores , Neoplasias de la Vejiga Urinaria/patologíaRESUMEN
A 48-year-old Chinese woman presenting with continuing dull pain in the right lower back and abdomen was found to have a tumor with extensive osseous metaplasia in the upper-middle pole of the right kidney. The excised neoplasm specimen revealed a 29 × 26 mm hard tumor with dense ossification. Histopathological examination of the tumor showed that it contained lamellar bone forming trabeculae intermingled and spherical or polygonal epithelial cells that contained slightly irregular nuclei with small nucleoli and abundant pink to clear cytoplasm. Clear cell renal cell carcinoma with extensive osseous metaplasia is a very rare occurrence.
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Carcinoma de Células Renales/patología , Neoplasias Renales/patología , Osificación Heterotópica/patología , Carcinoma de Células Renales/diagnóstico por imagen , Carcinoma de Células Renales/cirugía , Femenino , Humanos , Neoplasias Renales/diagnóstico por imagen , Neoplasias Renales/cirugía , Metaplasia , Persona de Mediana Edad , Nefrectomía , Osificación Heterotópica/diagnóstico por imagen , Osificación Heterotópica/cirugía , Tomografía Computarizada por Rayos XRESUMEN
MicroRNA (miR)-429 has been frequently reported to be downregulated in various tumors, including renal cell carcinoma (RCC), nasopharyngeal carcinoma, Ehrlich ascites tumor cells, gastric cancer, non-small cell lung cancer and endometrial endometrioid carcinoma. The present study investigated the effects of miR-429 on human RCC A498 and 786-O cells. Following transfection of cells with miR-429 mimics and scrambled control, MTT, cell migration, cell invasion and luciferase assays were performed. In addition, western blotting was performed in order to assess the expression of specificity protein 1 (Sp1), which was predicted to be a target of miR-429 by TargetScan. The present results revealed that miR-429 inhibited cell proliferation, migration and invasion of 786-O and A498 cells. In addition, the present results demonstrated that miR-429 overexpression downregulated Sp1 protein expression, which provides evidence that miR-429 may directly target Sp1 in RCC. These results suggest that miR-429 may be investigated for use as a predictive marker for early detection of tumor metastasis and blocking RCC cells from becoming invasive.
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The expression of microRNA335 (miR335) has been demonstrated to be downregulated in numerous types of cancer. Thus far, no previous studies have investigated the miR335 expression in bladder cancer. In the present study, the expression and effects of miR335 were assessed in bladder cancer. The results of the present study provided, to the best of our knowledge, the first evidence that miR335 is downregulated in the tumor tissue of patients with bladder cancer. Following transfection of miR335, MTT, cell migration and invasion, luciferase and western blot assays were conducted in bladder cancer cell lines. The results demonstrated that miR335 inhibited cell proliferation, migration and invasion in T24 and EJ cells. In addition, the results suggested that miR335 directly targets Rhoassociated protein kinase 1 (ROCK1) in bladder cancer. The present study provided a novel therapeutic target, the miR335/ROCK1 axis in bladder cancer. The suggested approach will be beneficial in developing an effective treatment against bladder cancer.
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Movimiento Celular , Proliferación Celular , Regulación hacia Abajo , Regulación Neoplásica de la Expresión Génica , MicroARNs/biosíntesis , Proteínas de Neoplasias/biosíntesis , ARN Neoplásico/biosíntesis , Neoplasias de la Vejiga Urinaria/metabolismo , Quinasas Asociadas a rho/biosíntesis , Anciano , Línea Celular Tumoral , Femenino , Humanos , Masculino , MicroARNs/genética , Persona de Mediana Edad , Invasividad Neoplásica , Proteínas de Neoplasias/genética , ARN Neoplásico/genética , Neoplasias de la Vejiga Urinaria/genética , Neoplasias de la Vejiga Urinaria/patología , Quinasas Asociadas a rho/genéticaRESUMEN
Transitional cell carcinoma (TCC) is the one of the most commonly observed types of cancer globally. The identification of novel disease-associated genes in TCC has had a significant effect on the diagnosis and treatment of bladder cancer; however, there may be a large number of novel genes that have not been identified. In the present study, the exomes of two individuals who were diagnosed with muscle-invasive TCC (MI-TCC) were sequenced to investigate potential variants. Subsequently, following algorithm and filter analysis, Sanger sequencing was used to validate the results of deep sequencing. Immunohistochemistry (IHC) was employed to observe the differences in HECT, C2 and WW domain-containing E3 ubiquitin protein ligase 1 (HECW1) protein expression between tumor tissues and para-carcinoma tissues. A total of 6 nonsynonymous mutation genes were identified in MI-TCC, identified as copine VII, RNA binding motif protein, X-linked-like 3, acyl-CoA synthetase medium-chain family member 2A, HECW1, zinc finger protein 273 and trichohyalin. Furthermore, 5 cases were identified to possess a HECW1 gene mutation in 61 MI-TCC specimens, and all of these were point mutations located at exon 11 on chromosome 7. The mutation categories of HECW1 had 4 missense mutations and 1 nonsense mutation. IHC revealed that HECW1 protein was expressed at significantly increased levels in MI-TCC compared with normal bladder urothelium (P<0.001). The present study provided a novel approach for investigating genetic changes in the MI-TCC exome, and identified the novel mutant gene HECW1, which may possess a significant role in the pathogenesis of TCC.
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MicroRNA-497 (miR-497) has been reported to be downregulated in certain types of cancer, including breast, gastric, endometrial, colorectal and prostate cancer as well as hepatocellular and nasopharyngeal carcinoma. The present study aimed to investigate the underlying mechanism of the tumor suppressor function of miR497 in prostate cancer. Following transfection with miR497, the DU145 and PC3 prostate cancer cell lines were subjected to Transwell migration and invasion assays, western blot analysis and a luciferase assay. It was revealed that miRNA497 inhibited the migration and invasion of prostate cancer cells. In addition, is was indicated that miRNA497 directly targets hepatomaderived growth factor (HDGF) in prostate cancer cells. These results suggested that restoration of miR497 and the resulting downregulation of HDFG may represent a promising therapeutic strategy for prostate cancer.
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Movimiento Celular , Péptidos y Proteínas de Señalización Intercelular/metabolismo , MicroARNs/metabolismo , Neoplasias de la Próstata/genética , Neoplasias de la Próstata/patología , Regiones no Traducidas 3'/genética , Secuencia de Bases , Línea Celular Tumoral , Biología Computacional , Regulación Neoplásica de la Expresión Génica , Humanos , Péptidos y Proteínas de Señalización Intercelular/genética , Masculino , MicroARNs/genética , Invasividad NeoplásicaRESUMEN
MicroRNA-204 (miR-204) has been reported to be frequently downregulated in various types of cancer, including renal, brain, ovary, hematological and colon cancer. The present study, investigated the effects of miR204 on renal cell carcinoma. Following transfection of miR204, an MTT assay, cell migration assay, cell invasion assay, western blot analysis and luciferase assay were performed in renal cell carcinoma cell lines. It was demonstrated that miR204 inhibits cell proliferation, migration and invasion in 786O and A498 cells. To the best of our knowledge, this study is the first to demonstrate that miR204 directly targets SOX4 in renal cell carcinoma. These results suggested that miR-204 may have value as a marker for the early detection of tumor metastasis and a therapeutic target preventing the invasion of renal cell carcinoma.
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Regulación hacia Abajo , MicroARNs/genética , MicroARNs/metabolismo , Factores de Transcripción SOXC/genética , Factores de Transcripción SOXC/metabolismo , Regulación hacia Arriba , Regiones no Traducidas 3' , Secuencia de Bases , Carcinoma de Células Renales/genética , Carcinoma de Células Renales/patología , Línea Celular Tumoral , Movimiento Celular , Proliferación Celular , Supervivencia Celular , Humanos , Neoplasias Renales/genética , Neoplasias Renales/patología , MicroARNs/antagonistas & inhibidores , Oligonucleótidos Antisentido/metabolismo , Interferencia de ARN , Factores de Transcripción SOXC/antagonistas & inhibidores , Alineación de SecuenciaRESUMEN
Dysregulation of B7-H3 has been observed in a variety of types of human cancers. In the present study, the mRNA expression level of B7-H3 was analyzed in bladder cancer by performing semi-quantitative reverse transcription-polymerase chain reaction on clinical specimens from transitional cell carcinomas (TCCs) and their normal adjacent tissues (NATs). Immunohistochemical analysis was performed to compare the protein expression level of B7-H3 in TCCs and the paired NATs. The present study indicated that the B7-H3 mRNA expression level was significantly higher in the TCC samples compared with the paired NAT samples. Furthermore, immunohistochemical analyses indicated that the B7-H3 protein expression level was significantly upregulated in the TCC samples compared with in the paired NAT samples, indicating that B7-H3 dysregulation may be important in the progression of bladder cancer.
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microRNA99a (miR99a) was reported to be among the most frequently downregulated miRNAs in numerous types of human cancers, including prostate, bladder, hepatocellular and ovarian carcinoma, squamous cell carcinoma of the tongue, squamous cell lung carcinoma as well as childhood adrenocortical tumors. The aim of the present study was to determine the effects of miRNA99a on cell proliferation, colony formation ability, migration and invasion in prostate cancer. Following transfection with miRNA99a, cell viability, colony formation, cell migration and cell invasion assays were performed on prostate cancer cell lines, as well as western blot analysis and luciferase assays. miRNA99a inhibited cell proliferation, colony formation ability, migration and invasion in DU145 and PC3 cells, therefore indicating that miRNA99a may have a tumor suppressive role in prostate cancer. In addition, the present study provided the first evidence that the mechanism of action of miRNA99a may proceed by directly targeting fibroblast growth factor receptor 3 in prostate cancer. In conclusion, the results of the present study suggested that miRNA99a may have potential use as a therapeutic target for the treatment of prostate cancer.
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MicroARNs/metabolismo , Receptor Tipo 3 de Factor de Crecimiento de Fibroblastos/metabolismo , Secuencia de Bases , Sitios de Unión , Línea Celular Tumoral , Movimiento Celular , Proliferación Celular , Supervivencia Celular , Regulación hacia Abajo , Humanos , Masculino , MicroARNs/genética , Neoplasias de la Próstata/metabolismo , Neoplasias de la Próstata/patología , ARN Bicatenario/metabolismo , Receptor Tipo 3 de Factor de Crecimiento de Fibroblastos/química , Receptor Tipo 3 de Factor de Crecimiento de Fibroblastos/genética , Alineación de Secuencia , TransfecciónRESUMEN
The expression of microRNA-99a (miRNA-99a) has been investigated in a number of human cancers. It has been reported to be downregulated in several types of cancer, including ovarian carcinoma, squamous cell carcinoma of the tongue, squamous cell lung carcinoma, hepatocellular carcinoma, bladder cancer, prostate cancer and childhood adrenocortical tumors. In the present study, the effects of miRNA-99a on bladder cancer cell proliferation, migration and invasion were examined. Following transfection of miRNA-99a, cell viability, cell migration assay, cell invasion, western blot analysis and luciferase assays were conducted in bladder cancer cell lines. It was found that miRNA-99a inhibits cell proliferation, migration and invasion in T24 and EJ cells. Additionally, this study provided the first evidence that miRNA-99a is likely to directly target fibroblast growth factor receptor 3 in bladder cancer. The study provided evidence that miRNA-99a suppresses cell proliferation, migration and invasion by targeting growth factor receptor 3 in bladder cancer cell lines. These results indicated that it could be investigated as a target for therapeutic drugs designed to treat bladder cancer.
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microRNA145 (miR145) has been reported to be frequently downregulated in various types of cancer, including renal, prostate, bladder, lung and colon cancer, as well as Bcell malignancies. The present study examined the effects of miR145 on the cell proliferation, migration and invasion of renal cell carcinoma (RCC). Following transfection of miR145, an MTT, cell migration, cell invasion and luciferase assays, and western blot analysis were conducted in RCC cell lines. The present study demonstrated that miR145 inhibited cell proliferation, migration and invasion in 786O and A498 cells. The present study also demonstrated for the first time, to the best of our knowledge, that miR145 may directly target matrix metallopeptidase11 (MMP11) in RCC. miR145 was demonstrated to suppress cell proliferation, migration and invasion by targeting MMP11 in RCC cell lines. These results suggested that it may be investigated as a predictive marker for the early detection of tumor metastasis and for targeting therapeutic drugs to inhibit the invasion of RCC.