Sandwich-Structured Flexible PVA/CS@MWCNTs Composite Films with High Thermal Conductivity and Excellent Electrical Insulation.

High thermal conductivity polymer matrix composites have become an urgent need for the thermal management of modern electronic devices. However, increasing the thermal conductivity of polymer-based composites typically results in loss of lightweight, flexibility and electrical insulation. Herein, the polyvinyl alcohol (PVA)/PVA-chitosan-adsorbed multi-walled carbon nanotubes/PVA (PVA/CS@MWCNTs) composite films with a sandwich structure were designed and fabricated by a self-construction strategy inspired by the surface film formation of milk. The obtained film simultaneously possesses high thermal conductivity, electrical insulation, and excellent flexibility. In this particular structure, the uniform intermediate layer of PVA-CS@MWCNTs contributed to improving the thermal conductivity of composite films, and the PVA distributed on both sides of the sandwich structure maintains the electrical insulation of the films (superior electrical resistivity above 1012 Ω·cm). It has been demonstrated that the fillers could be arranged in a horizontal direction during the scraping process. Thus, the obtained composite film exhibited high in-plane thermal conductivity of 5.312 W·m-1·K-1 at fairly low MWCNTs loading of 5 wt%, which increased by about 1190% compared with pure PVA (0.412 W·m-1·K-1). This work effectively realizes the combination of high thermal conductivity and excellent electrical insulation, which could greatly expand the application of polymer-based composite films in the area of thermal management.

NLRC3 High Expression Represents a Novel Predictor for Positive Overall Survival Correlated With CCL5 and CXCL9 in HCC Patients.

NLRC3 (NLR family caspase recruitment domain containing 3) has been reported as a factor of inhibiting inflammatory responses. It's role in HCC (hepatocellular carcinoma) is still unknown. In this study we firstly used the GEO (Gene Expression Omnibus) database and mIHC (multiple immunohistochemical analysis) with TMAs (tumor tissue microarrays) of HCC patients to evaluate NLRC3 levels. The tumor-bearing mouse models were also established with NLRC3 over-expressing and knock-down Hepal-6 cells to assess its effect. The data showed high NLRC3 expression was related with favorable overall survival (P=0.0386) and disease-free survival (P=0.0458). In addition, NLRC3 expression showed a positive correlation between CD8+ T cells infiltration. In vivo, NLRC3-overexpressing Hepal-6 tumors showed increased CD8+ T cell infiltration. NLRC3-knockdown Hepa1-6 tumors displayed decreased CD8+ T cell infiltration. At the same time, we also found the positive correlations between NLRC3 and CCL5 (C-C motif chemokine ligand 5, P<0.0001, R2 = 0.2372) as well as CXCL9 (C-X-C motif chemokine ligand 9, P<0.0001, R2 = 0.2338) expressions. So NLRC3 high expression represents a novel predictor for positive survival outcomes in HCC patients, and NLRC3 is involved in CD8+ T cell infiltration, which is correlated with increased CCL5 and CXCL9 in TME (tumor microenvironment). This study implies that boosting NLRC3 is a promising treatment to enhance survival in HCC patients.

miR-129-5p inhibits prostate cancer proliferation via targeting ETV1.

BACKGROUND: Prostate cancer is one of the most commonly diagnosed diseases in males. METHODS: RT-qPCR was used to detect miR-129-5p expression in tumor tissues and adjacent normal tissues from patients with prostate cancer. The cell proliferation assay and colony forming assay were used to study the role of miR-129-5p in mediating prostate cancer cell growth. Bioinformatic analysis and dual luciferase assay were performed to predict and confirm ETV1 as a target gene of miR-129-5p. RESULTS: We found that miR-129-5p levels were decreased significantly in human prostate cancer tissues compared with matched normal tissues from patients with prostate cancer. Overexpression of miR-129-5p suppressed prostate cancer cell growth while antagonist of miR-129-5p promoted cell proliferation in immortal prostate cell line RWPE-1. In addition, elevation of miR-129-5p decreased ETV1 expression in prostate cancer cells while downregulation of miR-129-5p increased ETV1 expression in RWPE-1. Mechanistically, ETV1 is confirmed a direct target of miR-129-5p in prostate cancer cells. Through repression of ETV1 expression, miR-129-5p could inactivate YAP signaling in prostate cancer cells. In addition, overexpression of ETV1 attenuated miR-129-5p induced cell proliferation in prostate cancer cells. Correlation analysis further revealed that there was a negative correlation between miR-129-5p levels and ETV1 mRNA levels in tumor tissues from patients with prostate cancer. CONCLUSION: Our results identified miR-129-5p as a tumor suppressor in prostate cancer via repression of ETV1.

Downregulation of miR-139-5p promotes prostate cancer progression through regulation of SOX5.

Altered expression of microRNAs (miRNAs) was involved in prostate cancer progression. However, how miRNAs contributed to prostate cancer development remained unknown. Here, we reported that miR-139-5p levels were decreased in prostate cancer tumor tissues and prostate cancer cell lines. Transfection of miR-139-5p mimics reduced cell proliferation and migration ability of prostate cancer cells. Western blotting and RT-qPCR showed that elevation of miR-139-5p greatly inhibited SOX5 expression in prostate cancer cells. Through regulation of SOX5, enhanced expression of miR-139-5p downregulated TWIST, decreased N-cadherin and Vimentin expression, suggesting inhibition of epithelial-mesenchymal transition (EMT) process. The dual luciferase assay validated that SOX5 was a direct target of miR-139-5p. Additionally, a significant negative correlation between SOX5 mRNA levels and miR-139-5p levels were detected in prostate cancer tumor tissues. Our study indicated that miR-139-5p functioned as a tumor suppressor in prostate cancer cells by regulation of SOX5, and it might be a promising target for prostate cancer patients.

Effect of adjuvant hormone therapy in patients with prostate cancer: A meta-analysis of randomized controlled trials.

OBJECTIVES: To summarize the evidence regarding the treatment effect of adjuvant hormone therapy (AHT) in patients with prostate cancer (PCa). AHT following radiotherapy, chemotherapy, or surgery is widely used in patients with PCa. However, the treatment effect is inconsistent in individual trials. METHODS: The electronic databases including PubMed, EmBase, and Cochrane Library were searched to identify randomized controlled trials (RCTs) in September 2016. RCTs that evaluated the effects of AHT in patients with PCa were included. Hazard ratio (HR) and relative risks (RR) were used to measure the treatment effects of AHT using a random effects model. The analyses were further stratified by factors that could affect the treatment efficacy. RESULTS: A total of 14,594 potential studies were identified, and 27 RCTs were included. Compared with the control group, patients who received AHT were associated with a significant improvement in overall survival (OS) (HR: 0.78; 95% confidence interval [CI]: 0.71-0.85; P <.001), disease-free survival (DFS) (HR: 0.50; 95% CI: 0.39-0.65; P <.001), total mortality (RR: 0.90; 95% CI: 0.85-0.96; P = .001), recurrence (RR: 0.70; 95% CI: 0.60-0.81; P <.001), and disease-specific mortality (RR: 0.70; 95% CI: 0.56-0.87; P <.001). However, no significant difference was observed between AHT and control for response rate (RR: 1.75; 95% CI: 0.91-3.37; P = .095). CONCLUSIONS: The findings of this meta-analysis confirmed that patients who received AHT had a significant improvement in OS, DFS, total mortality, recurrence, and disease-specific mortality. Further, large-scale RCTs are required to evaluate the treatment effect in specific subpopulations.

Laparoscopic versus open nephroureterectomy for upper urinary tract urothelial carcinoma: A systematic review and meta-analysis.

PURPOSE: To evaluate the efficacy and safety of laparoscopic nephroureterectomy (LNU) and open nephroureterectomy (ONU) for the treatment of upper urinary tract urothelial carcinoma (UTUC). METHODS: PubMed, Embase, and Cochrane databases were selected for systematic review of trials that compared outcomes of LNU and ONU. Meta-analysis was performed using RevMan 5.3 and STATA 13.0 software. RESULTS: LNU was associated with longer operation time (P < .001), shorter hospital stay (P < .001), less blood loss (P = .006) and lower rate of transfusion (P < .001). The occurrence of complications, including minor (P = .52), major (P = .21) and total complications (P = .19) were similar between LNU and ONU. There was no significant difference in the rate of 5-year recurrence-free survival (P = .90), 5-year cancer-specific survival (P = .12), and 5-year overall survival (P = .11) as well as 2-year RFS (P = .84), 2-year CSS (P = .86), and 2-year OS (P = .25). CONCLUSION: Our results indicated that LNU is a safe and effective method to treat UTUC. Given the limitations of this study, further multicenter, randomized trials are required to confirm these findings.

TUG1 promotes prostate cancer progression by acting as a ceRNA of miR-26a.

Previous studies have demonstrated that taurine-upregulated gene 1 (TUG1) was aberrantly expressed and involved in multiple types of cancer; however, the expression profile and potential role of TUG1 in prostate cancer (PCa) remains unclear. The aim of the present study was to evaluate the expression and function of TUG1 in PCa. In the present study, we analyzed TUG1 expression levels of PCa patients in tumor and adjacent normal tissue by real-time quantitative PCR. Knockdown of TUG1 by RNAi was performed to explore its roles in cell proliferation, migration, and invasion. Here we report, for the first time, that TUG1 promotes tumor cell migration, invasion, and proliferation in PCa by working in key aspects of biological behaviors. TUG1 could negatively regulate the expression of miR-26a in PCa cells. The bioinformatics prediction revealed putative miR-26a-binding sites within TUG1 transcripts. In conclusion, our study suggests that long non-coding RNA (lncRNA) TUG1 acts as a functional oncogene in PCa development.

Long non-coding RNA HOTTIP promotes prostate cancer cells proliferation and migration by sponging miR-216a-5p.

Long non-coding RNAs (lncRNAs) are a class of ncRNAs with >200 nts in length that regulate gene expression. The HOXA transcript at the distal tip (HOTTIP) lncRNA plays an important role in carcinogenesis, however, the underlying role of HOTTIP in prostate cancer (PCa) remains unknown. The aim of the present study was to evaluate the expression and function of HOTTIP in PCa. In the present study, we analyzed HOTTIP expression levels of 86 PCa patients in tumor and adjacent normal tissue by real-time quantitative PCR (qPCR). Knockdown or overexpression of HOTTIP was performed to explore its roles in cell proliferation, migration, invasion, and cell cycle. Furthermore, bioinformatics online programs predicted and luciferase reporter assay were used to validate the association of HOTTIP and miR-216a-5p in PCa cells. Our results found that HOTTIP was up-regulated in human primary PCa tissues with lymph node metastasis. Knockdown of HOTTIP inhibited PCa cell proliferation, migration, and invasion. Overexpression of HOTTIP promoted cell proliferation, migration, and invasion of PCa cells. Bioinformatics online programs predicted that HOTTIP sponge miR-216a-5p at 3'-UTR with complementary binding sites, which was validated using luciferase reporter assay. HOTTIP could negatively regulate the expression of miR-216a-5p in PCa cells. Above all, the knockdown of HOTTIP could represent a rational therapeutic strategy for PCa.

miR-671 promotes prostate cancer cell proliferation by targeting tumor suppressor SOX6.

Prostate cancer is one of the most severe malignancies in men, and many genes and non-coding RNAs, included microRNAs (miRs), have been demonstrated to regulate prostate cancer progression. In the present study, we investigated the role of miR-671 in prostate cancer cell proliferation. We found that miR-671 was significantly upregulated in human prostate cancer tissues and cells. miR-671 overexpression promoted prostate cancer cell proliferation, while its downregulation inhibited prostate cancer cell proliferation, as determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assays, colony formation assays, soft agar growth assays, and bromodeoxyuridine (BrdU) incorporation assays. miR-671 directly targets the 3' untranslated region (UTR) of the tumor suppressor SOX6 (encoding SRY (sex determining region Y)-box 6) to inhibit its expression. Double knockdown of miR-671 and SOX6 promoted PC3 cell proliferation, suggesting that miR-671 promotes prostate cancer cell proliferation by inhibiting SOX6.