Porous Copper Microspheres for Selective Production of Multicarbon Fuels via CO2 Electroreduction.

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.

Porous Cobalt-Nickel Hydroxide Nanosheets with Active Cobalt Ions for Overall Water Splitting.

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.

[Retracted] MicroRNA­143 inhibits cell migration and invasion by targeting matrix metalloproteinase 13 in prostate cancer.

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].

[Corrigendum] MicroRNA­335 is downregulated in bladder cancer and inhibits cell growth, migration and invasion via targeting ROCK1.

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].

microRNA-125b inhibits cell migration and invasion by targeting matrix metallopeptidase 13 in bladder cancer.

[This retracts the article DOI: 10.3892/ol.2013.1123.].

[Corrigendum] MicroRNA­379­5p plays a tumor­suppressive role in human bladder cancer growth and metastasis by directly targeting MDM2.

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].

miR-143 decreases prostate cancer cells proliferation and migration and enhances their sensitivity to docetaxel through suppression of KRAS.

MicroRNAs have been implicated in regulating diverse cellular pathways. Emerging evidence indicates that miR-143 plays causal roles in cancer tumorigenesis as a tumor suppress gene; however, its role in prostate cancer tumorigenesis remains largely unknown. The aims of this study were to verify the effect of miR-143 on proliferation and migration abilities of prostate cancer cells. The expression level of miR-143 and its target gene KRAS were measured by realtime PCR and western blotting, respectively. Effects of miR-143 in cell proliferation, migration and chemosensitivity were evaluated by MTT assay, FACS cell cycle analysis, colony formation assay, and transwell migratory assay. Our results revealed an inverse correlation of expression between miR-143 and KRAS protein in prostate cancer samples (Pearson's correlation scatter plots: R = -0.707, P < 0.05). Moreover, over-expression of miR-143 in prostate cancer cells suppressed their proliferation and migration and increased their sensitivity to docetaxel by targeting EGFR/RAS/MAPK pathway. These findings suggest that miR-143 plays an important role in prostate cancer proliferation, migration and chemosensitivity by suppressing KRAS and subsequent inactivation of MAPK pathway, which provides a potential development of a new approach for the treatment of prostate cancer.

Phosphatidylinositol 3-kinase inhibitor LY294002 suppresses proliferation and sensitizes doxorubicin chemotherapy in bladder cancer cells.

BACKGROUND: Phosphatidylinositol 3-kinase (PI3K)-AKT signaling is a well-characterized pathway involved in the control of cell proliferation, apoptosis and oncogenesis. LY294002 is a commonly used pharmacologic inhibitor which acts at the ATP-binding site of the PI3K enzyme, thus selectively inhibiting the PI3K-AKT nexus. The purpose of the present study was to examine whether PI3K inhibited by LY294002 had an effect on human bladder cancer cells. METHODS: After treatment with LY294002, MTT assay, chemosensitivity test, colony formation assay, apoptosis assay and Western blot analysis were conducted in EJ cells. RESULT: EJ cells treated with LY294002 showed significant AKT phosphorylation suppression in a dose-response manner. Also, PI3K/AKT signaling inhibitor LY294002 suppressed cell proliferation and enhanced the chemosensitivity of doxorubicin in human bladder cancer EJ cells. Furthermore, LY294002 increased cell apoptosis to doxorubicin. CONCLUSION: The augmentation of doxorubicin with PI3K inhibitor LY294002 may resolve the multidrug resistance of bladder cancer, and this may be a new strategy for achieving tolerance for chemotherapeutic agents in bladder cancer therapy.

Phosphatidylinositol 3-kinase inhibitor LY294002 suppresses proliferation and sensitizes doxorubicin chemotherapy in bladder cancer cells.

BACKGROUND: Phosphatidylinositol 3-kinase (PI3K)-AKT signaling is a well-characterized pathway involved in control of cell proliferation, apoptosis and oncogenesis. LY294002 is a commonly used pharmacologic inhibitor which acts at the ATP-binding site of the PI3K enzyme, and thus selectively inhibits the PI3K-AKT nexus. The purpose of the study was to examine whether PI3K inhibited by LY294002 had effects in human bladder cancer cells. METHODS: After treatment with LY294002, MTT assay, a chemosensitivity test, colony formation assay, apoptosis assay and Western blot analysis were conducted in EJ cells. RESULT: EJ cells treated with LY294002 showed significant AKT phosphorylation suppressing in a dose-response manner. Additionally, the PI3K/AKT signaling inhibitor LY294002 suppressed cell proliferation and enhanced chemosensitivity to doxorubicin in human bladder cancer EJ cells. Furthermore, LY294002 increased cell apoptosis to doxorubicin. CONCLUSION: The augmentation of doxorubicin with the PI3K inhibitor LY294002 may resolve the multidrug resistance of bladder cancer, and this may be a new strategy for achieving tolerance for chemotherapeutic agents in bladder cancer therapy.

A functional polymorphism in Pre-miR-146a gene is associated with prostate cancer risk and mature miR-146a expression in vivo.

BACKGROUND: A G > C polymorphism (rs2910164) which is located in the sequence of miR-146a precursor, results in a change from a G:U pair to a C:U mismatch in its stem region. To explore whether rs2910164 plays any role in prostate cancer (CaP), we analyzed the association between miR-146a polymorphism and risk of CaP and the expression of miR-146a with different genotypes in CaP tissues in southern Chinese Han population. MATERIALS AND METHODS: Two hundred fifty-one CaP and 280 control subjects were included in the cancer association study, and 15 CaP tissue samples were used to test the expression of the miRNA precursors by real-time quantitative reverse transcription PCR. RESULTS: We found that subjects carrying CC homozygotes had a 0.65-fold reduced risk (95% CI = 0.43-0.99) than those carrying GG/GC genotypes (P = 0.03), and the C allele displayed a lower prevalence of CaP compared with the G allele (OR = 0.73, 95% CI = 0.57-0.94, P = 0.01). Moreover, hsa-miR-146a quantification showed that homozygous carriers of the C-variant had significantly decreased miRNA levels compared to the carriers of the GG/GC genotype. CONCLUSIONS: The natural genetic variation in pre-miR-146a affects the amount of mature miR-146a, contributes to the genetic predisposition to CaP.

Long noncoding RNA NNT-AS1 enhances the malignant phenotype of bladder cancer by acting as a competing endogenous RNA on microRNA-496 thereby increasing HMGB1 expression.

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.

Lattice-strained palladium nanoparticles as active catalysts for the oxygen reduction reaction.

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.

Bond-Energy-Integrated Descriptor for Oxygen Electrocatalysis of Transition Metal Oxides.

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.

Clear Cell Renal Cell Carcinoma With Extensive Osseous Metaplasia: Report of a Rare Case.

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.

MicroRNA-379-5p plays a tumor-suppressive role in human bladder cancer growth and metastasis by directly targeting MDM2.

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.

MicroRNA-335 is downregulated in bladder cancer and inhibits cell growth, migration and invasion via targeting ROCK1.

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.

MicroRNA-497 targets hepatoma-derived growth factor and suppresses human prostate cancer cell motility.

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.

Tumor-suppressing effects of microRNA-429 in human renal cell carcinoma via the downregulation of Sp1.

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.

Novel somatic mutations identified by whole-exome sequencing in muscle-invasive transitional cell carcinoma of the bladder.

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.

microRNA­99a inhibits cell proliferation, colony formation ability, migration and invasion by targeting fibroblast growth factor receptor 3 in prostate cancer.

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.