Achieving High Initial Coulombic Efficiency and Capacity in a Surface Chemical Grafting Layer of Plateau-type Sodium Titanate.

The plateau-type sodium titanate with suitable sodiation potential is a promising anode candidate for high safe and high energy density of sodium-ion batteries (SIBs). However, the poor initial Coulombic efficiency (ICE) and cyclic instability of sodium titanate are attributed to the unstable interfacial structure along with the decomposition of electrolytes, resulting in the continuous formation of solid electrolyte interface (SEI) film. To address this issue, a chemical grafting method is developed to fabricate a highly stable interface layer of inert Al2O3 on the sodium titanate anode, rendering the high ICE and excellent cycling stability. Based on theoretical calculations, NaPF6 are more likely adsorption on the Al2O3 surface and produce sodium fluoride. The formation of a thin and dense SEI film with rich sodium fluoride achieves the low interfacial resistances and charge-transfer resistances. Benefitting from our design, the obtained sodium titanate exhibits a high ICE from 67.7 % to 79.4 % and an enhanced reversible capacity from 151 mAh g-1 to 181 mAh g-1 at 20 mA g-1, along with an increase in capacity retention from 56.5 % to 80.6 % after 500 cycles. This work heralds a promising paradigm for rational regulation of interfacial stability to achieve high-performance anodes for SIBs.

Enhancement of acid tolerance of Escherichia coli by introduction of molecule chaperone CbpA from extremophile.

Molecular chaperone CbpA from extreme acidophile Acidithiobacillus caldus was applied to improve acid tolerance of Escherichia coli via CRISPR/Cas9. Cell growth and viability of plasmid complementary strain indicated the importance of cbpAAc for bacteria acid tolerance. With in situ gene replacement by CRISPR/Cas9 system, colony formation unit (CFU) of genome recombinant strain BL21-ΔcbpA/AccbpA showed 7.7 times higher cell viability than deficient strain BL21-ΔcbpA and 2.3 times higher than wild type. Cell morphology observation using Field Emission Scanning Electron Microscopy (FESEM) revealed cell breakage of BL21-ΔcbpA and significant recovery of BL21-ΔcbpA/AccbpA. The intracellular ATP level of all strains gradually decreased along with the increased stress time. Particularly, the value of recombinant strain was 56.0% lower than that of deficient strain after 5 h, indicating that the recombinant strain consumed a lot of energy to resist acid stress. The arginine concentration in BL21-ΔcbpA/AccbpA was double that of BL21-ΔcbpA, while the aspartate and glutamate contents were 14.8% and 6.2% higher, respectively, compared to that of wild type. Moreover, RNA-Seq analysis examined 93 genes down-regulated in BL21-ΔcbpA compared to wild type strain, while 123 genes were up-regulated in BL21-ΔcbpA/AccbpA compared to BL21-ΔcbpA, with an emphasis on energy metabolism, transport, and cell components. Finally, the working model in response to acid stress of cbpA from A. caldus was developed. This study constructed a recombinant strain resistant to acid stress and also provided a reference for enhancing microorganisms' robustness to various conditions.

Evaluation of Image Quality and Detectability of Deep Learning Image Reconstruction (DLIR) Algorithm in Single- and Dual-energy CT.

This study is aimed to evaluate effects of deep learning image reconstruction (DLIR) on image quality in single-energy CT (SECT) and dual-energy CT (DECT), in reference to adaptive statistical iterative reconstruction-V (ASIR-V). The Gammex 464 phantom was scanned in SECT and DECT modes at three dose levels (5, 10, and 20 mGy). Raw data were reconstructed using six algorithms: filtered back-projection (FBP), ASIR-V at 40% (AV-40) and 100% (AV-100) strength, and DLIR at low (DLIR-L), medium (DLIR-M), and high strength (DLIR-H), to generate SECT 120kVp images and DECT 120kVp-like images. Objective image quality metrics were computed, including noise power spectrum (NPS), task transfer function (TTF), and detectability index (d'). Subjective image quality evaluation, including image noise, texture, sharpness, overall quality, and low- and high-contrast detectability, was performed by six readers. DLIR-H reduced overall noise magnitudes from FBP by 55.2% in a more balanced way of low and high frequency ranges comparing to AV-40, and improved the TTF values at 50% for acrylic inserts by average percentages of 18.32%. Comparing to SECT 20 mGy AV-40 images, the DECT 10 mGy DLIR-H images showed 20.90% and 7.75% improvement in d' for the small-object high-contrast and large-object low-contrast tasks, respectively. Subjective evaluation showed higher image quality and better detectability. At 50% of the radiation dose level, DECT with DLIR-H yields a gain in objective detectability index compared to full-dose AV-40 SECT images used in daily practice.

ncRNA-mediated overexpression of ubiquitin-specific proteinase 13 contributes to the progression of prostate cancer via modulating AR signaling, DNA damage repair and immune infiltration.

Metastatic castration-resistant prostate cancer (mCRPC) is a lethal form of prostate cancer, and the molecular mechanism driving mCRPC progression has not yet been fully elucidated. Immunotherapies such as chimeric antigen receptor, T-cell therapy and immune checkpoint blockade have exerted promising antitumor effects in hematological and solid tumor malignancies; however, no encouraging responses have been observed against mCRPC. The deubiquitinase USP13 functions as a tumor suppressor in many human cancers, as it sustains the protein stability of PTEN and TP53; however, its role in prostate cancer (PCa) and involvement in DNA damage and AR signaling remain unclear. In the current study, we explored the prognostic value of USP13 in PCa based on the TCGA database, and we analyzed the expression of USP13 in PCa tissues and adjacent normal tissues based on TCGA and our cohort. The results suggested that USP13 is overexpressed in PCa tumors and has the potential to be an independent biomarker for the overall survival of PCa patients. Additionally, enrichment analysis indicated that USP13 may participate in the AR pathway and PI3k/Wnt signaling, which are closely related to PCa progression. We also observed a significant correlation between the expression of USP13 and AR-related genes, DDR genes and mismatch repair genes based on the TCGA_PRAD dataset, which further supported the critical role of USP13 in AR activation and the DNA damage response of PCa. USP13 was also found to be enriched in protein neddylation, and expression of USP13 was significantly associated with infiltration of immune cells and expression of immunomodulators. Taken together, our study revealed a key role of USP13 in contributing to PCa progression by participating in multiple oncogenic signaling pathways, the DNA damage response and the immunosuppressive tumor microenvironment. Targeting USP13 may inhibit tumor growth and provide additional benefits in cooperation with DDR inhibitors and immunotherapy.

Integrative Analysis and Experimental Validation Indicated That SNHG17 Is a Prognostic Marker in Prostate Cancer and a Modulator of the Tumor Microenvironment via a Competitive Endogenous RNA Regulatory Network.

The incidence of prostate cancer (PC) is growing rapidly worldwide, and studies uncovering the molecular mechanisms driving the progression and modulating the immune infiltration and antitumor immunity of PC are urgently needed. The long noncoding RNA SNHG family has been recognized as a prognostic marker in cancers and contributes to the progression of multiple cancers, including PC. In this study, we aimed to clarify the prognostic values and underlying mechanisms of SNHGs in promoting the progression and modulating the tumor microenvironment of PC through data mining based on The Cancer Genome Atlas (TCGA) database. We identified that within the SNHG family, SNHG17 was most correlated with the overall survival of PC patients and could act as an independent predictor. Moreover, we constructed a competitive endogenous RNA (ceRNA) network by which SNHG17 promotes progression and potentially inhibits the immune infiltration and immune response of prostate cancer. By interacting with miR-23a-3p/23b-3p/23c, SNHG17 upregulates the expression of UBE2M and OTUB1, which have been demonstrated to play critical roles in the tumorigenesis of human cancers, more importantly promoting cancer cell immunosuppression and resistance to cytotoxic stimulation. Finally, we examined the correlation between SNHG17 expression and the clinical progression of PC patients based on our cohort of 52 PC patients. We also verified the SNHG17/miR-23a/OTUB1 axis in RV-1 and PC-3 cells by dual luciferase and RIP assays, and we further identified that SNHG17 promoted cellular invasive capacity by modulating OTUB1. In summary, the current study conducted a ceRNA-based SNHG17-UBE2M/OTUB1 axis and indicated that SNHG17 might be a novel prognostic factor associated with the progression, immunosuppression, and cytotoxic resistance of PC.

The Changes of Gene Expression and Protein Level of Stretch-Activated Chloride Channel in Atrial Myocardium of Dogs with Atrial Fibrillation.

INTRODUCTION: ICl,stretch have been reported to be involved in the development of atrial fibrillation, so we observed the changes of transcription and translation levels of ICl,stretch in isolated atrial myocardium of heart failure canine models. MATERIAL AND METHODS: In the control group (N = 10), five dogs were untreated and the other five received sham operation, while dogs in the heart failure group (N = 10) were implanted with cardiac pacemakers and underwent right ventricular pacing to induce heart failure. Cardiac structure and function were evaluated. The gene expression and protein level of ICl,stretch in the left atrial appendage were detected. RESULTS: The left atrial diameter, right atrial dimension, left ventricular diastolic dimension, and right ventricular diastolic dimension were significantly larger in the heart failure group (P < 0.05). In contrast, the ejection fraction and the left ventricular shorten fraction were higher in the control group (P < 0.05). Both the mRNA and protein expression levels of ICl,stretch in atrial myocardium of the heart failure group were significantly higher compared with the control group. CONCLUSION: ICl,stretch might play an important role in the vulnerability to atrial fibrillation in dilated atria with heart failure and could be a potential therapeutic target for atrial fibrillation.

Simultaneous denitrification and desulfurization-S0 recovery of wastewater in trickling filters by bioaugmentation intervention based on avoiding collapse critical points.

In order to better achieve efficiently simultaneous desulfurization and denitrification/S0 recovery of wastewater, the intervention of sulfur oxidizing bacteria (SOB) and denitrifying bacteria (DNB) was employed to avoid the collapse critical points (the dramatically decrease of S/N removal efficiency) under the fluctuated load. With the assistance of DNB and SOB, collapse critical point of trickling filter (TF) was delayed from the P8 (105-114 d) to P10 stage (129-138 d). The treatment efficiency of nitrogen and sulfur was the highest with the S/N ratio of 3:1. The bioaugmentation of DNB and SOB at collapse critical point could effectively regulated collapse situation, which further increased the maximum system utilization/elimination capacity to 4.50 kg S m-3·h-1 and 0.90 kg N m-3·h-1 (increased by 56.89% and 65.56% in comparison to control). High-throughput sequencing analysis indicated that Proteobacteria (average 78.59%) and Bacteroidetes (average 9.30%) were dominant bacteria in the reactor at all stages. As the reaction proceeds, the microbial community was gradually dominated by some functional genera such as Chryseobacterium (average 2.97%), Halothiobacillus (average 22.71%), Rhodanobacter (average 14.02%), Thiobacillus (average 9.01%), Thiomonas (average 16.70%) and Metallibacterium (average 21.63%), which could remove nitrate or sulfide. Both of Principal Component Analysis (PCA) and Canonical Correlation Analysis (CCA) demonstrated the important role of DNB/SOB during the long-term run in the trickling filters (TFs).

microRNA-1271 impedes the development of prostate cancer by downregulating PES1 and upregulating ERß.

BACKGROUND: As a nucleolar protein associated with ribosome biogenesis, pescadillo homolog 1 (PES1) has been reported to participate in the development of many cancers. However, its role in prostate cancer is not clearly defined. Therefore, the aim of this study is to explore the effects and the specific mechanism of PES1 in prostate cancer. METHODS: A microarray-based analysis was performed to analyze differentially expressed genes (DEGs) between prostate cancer and normal samples. Next, the interaction between PES1 and microRNA-1271 (miR-1271) was investigated using bioinformatics analysis in combination with dual-luciferase reporter gene assay. The expression of miR-1271 in prostate cancer cells and tissues was determined using RT-qPCR. Its effects on downstream estrogen receptor ß (ERß) signaling pathway were further examined. Moreover, we analyzed whether miR-1271 affects proliferation, apoptosis, migration and invasion of prostate cancer cells by EdU assay, flow cytometry, and Transwell assay. Lastly, a prostate cancer mouse model was conducted to measure their roles in the tumor growth. RESULTS: PES1 was identified as a prostate cancer-related DEG and found to be upregulated in prostate cancer. miR-1271, which was poorly expressed in both cells and tissues of prostate cancer, can specifically bind to PES1. Additionally, overexpression of miR-1271 activated the ERß signaling pathway. Overexpression of miR-1271 or depletion of PES1 inhibited prostate cancer cell proliferation, migration and invasion, promoted apoptosis in vitro and suppressed tumor growth in vivo. CONCLUSIONS: Taken together, overexpression of miR-1271 downregulates PES1 to activate the ERß signaling pathway, leading to the delayed prostate cancer development. Our data highlights the potential of miR-1271 as a novel biomarker for the treatment of prostate cancer.

Long non-coding RNA LINC00673 silencing inhibits proliferation and drug resistance of prostate cancer cells via decreasing KLF4 promoter methylation.

Prostate cancer is one of the major causes of cancer-related mortality in men across the world. Recently, long non-coding RNAs (lncRNAs) and Kruppel-like factor 4 (KLF4) have been reported to participate in the biology of multiple cancers including prostate cancer. Here, this study aimed to explore the possible role of LINC00673 in prostate cancer via KLF4 gene promoter methylation. Microarray-based gene expression profiling of prostate cancer was employed to identify differentially expressed lncRNAs and genes, after which the expression of LINC00673 and KLF4 in prostate cancer tissues was determined using RT-qPCR. Next, the relationship between LINC00673 and KLF4 was evaluated using in silico analysis. Further, the effect of LINC00673 and KLF4 on cell proliferation and drug resistance of transfected cells was examined with gain- and loss-of-function experimentation. It was found that LINC00673 was highly expressed, while KLF4 was poorly expressed in prostate cancer tissues. Additionally, LINC00673 could bind to KLF4 gene promoter region and recruit methyltransferase to the KLF4 gene promoter region. Moreover, LINC00673 silencing was demonstrated to reduce methylation of the KLF4 gene promoter to elevate the expression of KLF4, thus suppressing the proliferation and drug resistance of prostate cancer cells. In summary, LINC00673 silencing could drive demethylation of the KLF4 gene promoter and thus inhibit the proliferation and drug resistance of prostate cancer cells, suggesting that silencing of LINC00673 and elevation of KLF4 could serve as tumour suppressors in prostate cancer.

Long noncoding RNA RBMS3-AS3 acts as a microRNA-4534 sponge to inhibit the progression of prostate cancer by upregulating VASH1.

Long noncoding RNAs (lncRNAs) have been demonstrated to participate in the progression of many malignancies, including prostate cancer by serving as sponges of microRNAs (miRNAs). Initial microarray-based analysis screened out the poorly expressed lncRNA RBMS3-AS3 in prostate cancer, followed by the identification of putative binding sites with miR-4534 and its target VASH1. Therefore, the present study set out to investigate the potential role of RBMS3-AS3/miR-4534/VASH1 axis in the development of prostate cancer. The biological functions of RBMS3-AS3, miR-4534, and VASH1 on cell proliferation, migration, invasion, and angiogenesis of prostate cancer were evaluated via gain- and loss-of-function experiments. Furthermore, tumor xenograft in nude mice was performed to examine tumorigenesis in vivo. The obtained results indicated that RBMS3-AS3 was poorly expressed in prostate cancer tissues and cells. Of note, overexpression of RBMS3-AS3 was found to suppress cell proliferation, migration, invasion, and angiogenesis as well as the tumorigenic ability of prostate cancer. VASH1 was verified as a target gene of miR-4534. VASH1 expression was found to be downregulated in prostate cancer tissues and cells. Interestingly, RBMS3-AS3 was observed to competitively bind to miR-4534 to upregulate VASH1 expression, resulting in a suppressive role in prostate cancer development. Also, in vitro findings were reproduced in vivo on tumor xenograft in nude mice. Taken together, the present study provides evidence suggesting that RBMS3-AS3 acts as a miR-4534 sponge to inhibit the development of prostate cancer by upregulating VASH1, highlighting a theoretical target for prostate cancer treatment.

Inactivation of the Wnt/ß-catenin signaling pathway underlies inhibitory role of microRNA-129-5p in epithelial-mesenchymal transition and angiogenesis of prostate cancer by targeting ZIC2.

Background: Prostate cancer (PCa) is a common disease that often occurs among older men and a frequent cause of malignancy associated death in this group. microRNA (miR)-129-5p has been identified as an essential regulator with a significant role in the prognosis of PC. Therefore, this study aimed to investigate roles of miR-129-5p in PCa. Methods: Microarray analysis was conducted to identify PCa-related genes. The expression of miR-129-5p and ZIC2 in PCa tissues was investigated. To understand the role of miR-129-5p and ZIC2 in PCa, DU145 cells were transfected with mimic or inhibitor of miR-129-5p, or si-ZIC2 and the expression of Wnt, ß-catenin, E-cadherin, vimentin, N-cadherin, vascular endothelial growth factor (VEGF), and CD31, as well as the extent of ß-catenin phosphorylation was determined. In addition, cell proliferation, migration, invasion, angiogenesis, apoptosis and tumorigenesis were detected. Results: miR-129-5p was poorly expressed and ZIC2 was highly expressed in PCa tissues. Down-regulation of ZIC2 or overexpression of miR-129-5p reduced the expression of ZIC2, Wnt, ß-catenin, N-cadherin, vimentin, and ß-catenin phosphorylation but increased the expression of E-cadherin. Importantly, miR-129-5p overexpression significantly reduced cell migration, invasion, angiogenesis and tumorigenesis while increasing cell apoptosis. Conclusions: The findings of the present study indicated that overexpression of miR-129-5p or silencing of ZIC2 could inhibit epithelial-mesenchymal transition (EMT) and angiogenesis in PCa through blockage of the Wnt/ß-catenin signaling pathway.

Elevated Swelling-Activated Chloride Current Densities in Hypertrophied Ventricular Myocytes in a Rabbit Heart Failure Model.

BACKGROUND: The status of the swelling-activated chloride channel (ICl, swell) during heart failure remains unclear. This study aimed to investigate whether the ICl, swell activity is altered during heart failure and to determine how the ICl, swell influences atrial arrhythmias of the failing heart. METHODS: We established a heart failure rabbit model and analyzed the hemodynamic indicators 8 weeks after myocardial infarction, which include left ventricular systolic pressure (LVSP) and left ventricular end-diastolic pressure (LVDEP). Five untreated rabbits and 5 receiving a sham operation served as the control group. Left auricular appendage tissues were obtained and CLCN3 mRNA/CLCN3 protein expression levels were examined by using reverse transcription-polymerase chain reaction and Western blot, respectively. RESULTS: Compared to the control group, the heart failure group showed a significantly decreased LVSP (14.2 ± 0.27 versus 16.9 ± 0.86 kPa, P <.05)and elevated LVDEP (2.49 ± 0.30 versus 0.15 ± 0.03 kPa, P <.05), indicating that myocardial infarction leads to progressive heart failure of rabbits in the heart failure group. CLCN3 mRNA and CLCN3 protein expression were both significantly elevated in the heart failure group compared to the control group (P <.05). CONCLUSION: In sum, we propose that the dynamic nature of ICl, swell upregulation may contribute to the elevated expression of CLCN3 mRNA and CLCN3 protein, resulting in myocardial cell remodeling induced by heart failure. However, further study is needed to investigate the potential functions of ICl, swell, especially the relation between ICl, swell augmentation and arrhythmia after heart failure.

Acute toxicity assessment of explosive-contaminated soil extracting solution by luminescent bacteria assays.

Explosive-contaminated soil is harmful to people's health and the local ecosystem. The acute toxicity of its extracting solution was tested by bacterial luminescence assay using three kinds of luminescent bacteria to characterize the toxicity of the soil. An orthogonal test L 16 (45) was designed to optimize the soil extracting conditions. The optimum extracting conditions were obtained when the ultrasonic extraction time, ultrasonic extraction temperature, and the extraction repeat times were 6 h, 40 °C, and three, respectively. Fourier transform infrared spectroscopy (FTIR) results showed that the main components of the contaminated soil's extracting solution were 2,4-dinitrotoluene-3-sulfonate (2,4-DNT-3-SO3-); 2,4-dinitrotoluene-5-sulfonate (2,4-DNT-5-SO3-); and 2,6-dinitrotoluene (2,6-DNT). Compared with Photobacterium phosphoreum and Vibrio fischeri, Vibrio qinghaiensis sp. Nov. is more suitable for assessing the soil extracting solution's acute toxicity. Soil washing can remove most of the contaminants toxic to luminescent bacterium Vibrio qinghaiensis sp. Nov., suggesting that it may be a potential effective remediation method for explosive-contaminated soil.

miR-130b, an onco-miRNA in bladder cancer, is directly regulated by NF-κB and sustains NF-κB activation by decreasing Cylindromatosis expression.

Persistent activation of NF-κB signaling is closely related to chronic inflammation and tumorigenesis. Commonly, NF-κB signaling is tightly controlled by multiple feedback loops and regulators, such as the deubiquitinases (DUBs). However, in cancer cells, NF-κB may override these feedbacks through special pathways and lead to the sustained activation. In the present study, we demonstrate that in transitional cell carcinoma (TCC) of bladder, miR-130b plays an oncogenesis role, it enhanced proliferation, invasion and migration of TCC cell, and was highly correlated with tumor progression. On the other hand, NF-κB directly regulated the transcription of miR-130b by binding with its promoter region. Importantly, we verify that, through deceasing the expression of Cylindromatosis (CYLD), a K63-specific DUB and endogenous blocker of NF-κB signaling, miR-130b can in return sustain the persistent activation of NF-κB, which may promote the malignant progression of TCC. Thus, the present study uncovers a potential signaling transduction in which NF-κB is continuously activated, and may provide a novel therapeutic approach for the clinical management of TCC.

Regulation of seminiferous tubule-associated stem Leydig cells in adult rat testes.

Testicular Leydig cells are the primary source of testosterone in males. Adult Leydig cells have been shown to arise from stem cells present in the neonatal testis. Once established, adult Leydig cells turn over only slowly during adult life, but when these cells are eliminated experimentally from the adult testis, new Leydig cells rapidly reappear. As in the neonatal testis, stem cells in the adult testis are presumed to be the source of the new Leydig cells. As yet, the mechanisms involved in regulating the proliferation and differentiation of these stem cells remain unknown. We developed a unique in vitro system of cultured seminiferous tubules to assess the ability of factors from the seminiferous tubules to regulate the proliferation of the tubule-associated stem cells, and their subsequent entry into the Leydig cell lineage. The proliferation of the stem Leydig cells was stimulated by paracrine factors including Desert hedgehog (DHH), basic fibroblast growth factor (FGF2), platelet-derived growth factor (PDGF), and activin. Suppression of proliferation occurred with transforming growth factor ß (TGF-ß). The differentiation of the stem cells was regulated positively by DHH, lithium- induced signaling, and activin, and negatively by TGF-ß, PDGFBB, and FGF2. DHH functioned as a commitment factor, inducing the transition of stem cells to the progenitor stage and thus into the Leydig cell lineage. Additionally, CD90 (Thy1) was found to be a unique stem cell surface marker that was used to obtain purified stem cells by flow cytometry.

Treatment of soil eluate containing nitro aromatic compounds by adsorption on activated coke (AC).

Soil washing is a kind of physical method to remove organic matters from contaminated soil. However, its eluate after washing may result in secondary pollution to the environment. In this study, activated coke (AC) was used to remove organic pollutants from contaminated soil eluate. The effect of temperature, initial chemical oxygen demand (COD) and AC dosage on COD removal efficiency was investigated. The results showed that the organic matter can be removed in the eluate because the COD dropped a lot. When the AC dosage was 20 g·L(-1), 88.92% of COD decreased after 480 min of adsorption at 50 °C. The process of adsorption can be described by the Redlich-Peterson isotherm. The adsorption was spontaneous and endothermic. The pseudo-second-order model can be used to describe the adsorption process. After adsorption, the acute toxicity of the eluate was reduced by 76%, and the water qualities were in agreement with Chinese discharge standard GB 14470.1-2002, which means the eluate could be discharged to the environment.

Reduction of protein kinase C α (PKC-α) promote apoptosis via down-regulation of Dicer in bladder cancer.

In clinic, we examined the expression of protein kinase C (PKC)-α and Dicer in the samples of bladder cancer patients, and found that the two proteins have a line correlation. Our study confirmed this correlation existing by clearing the decreasing expression of Dicer after the PKC-α knockdown. Treatment of bladder cancer cell lines (T24, 5637) with the PKC-α or Dicer knockdown and the PKC inhibitors (Calphostin C and Gö 6976) can promote the apoptosis. Inhibition of PKC can increase the activities of caspase-3 and PARP, however, decrease the expression of Dicer. And knockdown of the PKC-α or Dicer can also activate the caspase-3 or the PARP. Considering the reduction of PKC-α can induce the Dicer down-regulation, we make the conclusion that the reduction of PKC-α can promote the apoptosis via the down-regulation of Dicer in bladder cancer.

Aplasia Ras homolog member I expression induces apoptosis in renal cancer cells via the ß-catenin signaling pathway.

In numerous types of cancer, the Ras-associated tumor suppressor gene aplasia Ras homolog member I (ARHI), is downregulated. However, the function of ARHI in renal cancer remains to be elucidated. The present study investigated whether the suppressor gene ARHI influenced the growth of renal cancer cell lines and aimed to elucidate its mechanism of action, using the techniques of cell biology and molecular pathology. To the best of our knowledge, the present study was the first to determine the effects of ARHI on human renal cancer cells in vivo and in vitro. It was demonstrated that ARHI exhibited a tumor suppressor function in OS-RC-2 cells and acted via the ß-catenin signaling pathway. It was additionally confirmed that the levels of ARHI messenger RNA and protein in renal cancer tissues were lower than those in matched normal tissues. These results provided a novel insight into the possible therapeutic applications of ARHI in renal cancer.