Prediction of Prostate Cancer Risk Stratification Based on A Nonlinear Transformation Stacking Learning Strategy.

PURPOSE: Prostate cancer (PCa) is an epithelial malignancy that originates in the prostate gland and is generally categorized into low, intermediate, and high-risk groups. The primary diagnostic indicator for PCa is the measurement of serum prostate-specific antigen (PSA) values. However, reliance on PSA levels can result in false positives, leading to unnecessary biopsies and an increased risk of invasive injuries. Therefore, it is imperative to develop an efficient and accurate method for PCa risk stratification. Many recent studies on PCa risk stratification based on clinical data have employed a binary classification, distinguishing between low to intermediate and high risk. In this paper, we propose a novel machine learning (ML) approach utilizing a stacking learning strategy for predicting the tripartite risk stratification of PCa. METHODS: Clinical records, featuring attributes selected using the lasso method, were utilized with 5 ML classifiers. The outputs of these classifiers underwent transformation by various nonlinear transformers and were then concatenated with the lasso-selected features, resulting in a set of new features. A stacking learning strategy, integrating different ML classifiers, was developed based on these new features. RESULTS: Our proposed approach demonstrated superior performance, achieving an accuracy of 0.83 and an area under the receiver operating characteristic curve value of 0.88 in a dataset comprising 197 PCa patients with 42 clinical characteristics. CONCLUSION: This study aimed to improve clinicians' ability to rapidly assess PCa risk stratification while reducing the burden on patients. This was achieved by using artificial intelligence-related technologies as an auxiliary method for diagnosing PCa.

Multimodality deep learning radiomics nomogram for preoperative prediction of malignancy of breast cancer: a multicenter study.

Background. Breast cancer is the most prevalent cancer diagnosed in women worldwide. Accurately and efficiently stratifying the risk is an essential step in achieving precision medicine prior to treatment. This study aimed to construct and validate a nomogram based on radiomics and deep learning for preoperative prediction of the malignancy of breast cancer (MBC).Methods. The clinical and ultrasound imaging data, including brightness mode (B-mode) and color Doppler flow imaging, of 611 breast cancer patients from multiple hospitals in China were retrospectively analyzed. Patients were divided into one primary cohort (PC), one validation cohort (VC) and two test cohorts (TC1 and TC2). A multimodality deep learning radiomics nomogram (DLRN) was constructed for predicting the MBC. The performance of the proposed DLRN was comprehensively assessed and compared with three unimodal models via the calibration curve, the area under the curve (AUC) of receiver operating characteristics and the decision curve analysis.Results. The DLRN discriminated well between the MBC in all cohorts [overall AUC (95% confidence interval): 0.983 (0.973-0.993), 0.972 (0.952-0.993), 0.897 (0.823-0.971), and 0.993 (0.977-1.000) on the PC, VC, test cohorts1 (TC1) and test cohorts2 TC2 respectively]. In addition, the DLRN performed significantly better than three unimodal models and had good clinical utility.Conclusion. The DLRN demonstrates good discriminatory ability in the preoperative prediction of MBC, can better reveal the potential associations between clinical characteristics, ultrasound imaging features and disease pathology, and can facilitate the development of computer-aided diagnosis systems for breast cancer patients. Our code is available publicly in the repository athttps://github.com/wupeiyan/MDLRN.

HCR/DNAzyme-triggered cascaded feedback cycle amplification for self-powered dual-photoelectrode detection of femtomolar HPV16.

For high-performance dual-photoelectrode assay, developing a pair of photoactive materials with well-matched band structure and the design of a powerful sensing strategy are highly desirable. Herein, the Zn-TBAPy pyrene-based MOF and BiVO4/Ti3C2 Schottky junction were employed as photocathode and photoanode to form an efficient dual-photoelectrode system. The integration of the cascaded hybridization chain reaction (HCR)/DNAzyme-assisted feedback amplification with DNA walker-mediated cycle amplification strategy realizes femtomolar HPV16 dual-photoelectrode bioassay. Through the activation of the HCR cascaded with the DNAzyme system in the presence of HPV16, plentiful HPV16 analogs are generated that leads to exponential positive feedback signal amplification. Meanwhile on the Zn-TBAPy photocathode, the NDNA hybridizes with the bipedal DNA walker followed by circular cleavage by Nb.BbvCI NEase, producing a dramatically enhanced PEC readout. The achieved ultralow detection limit of 0.57 fM and a wide linear range of 10-6 nM-103 nM showcase the excellent performance of the developed dual-photoelectrode system.

Isolation, structural and bioactivities of polysaccharides from Anoectochilus roxburghii (Wall.) Lindl.: A review.

Anoectochilus roxburghii (Wall.) Lindl. (A. roxburghii), a valuable herbal medicine in China, has great medicinal and edible value. Polysaccharides, as one of the main active components of A. roxburghii, comprise glucose, arabinose, xylose, galactose, rhamnose, and mannose in different molar ratios and glycosidic bond types. By varying the sources and extraction methods of A. roxburghii polysaccharides (ARPS), different structural characteristics and pharmacological activities can be elucidated. ARPS has been reported to exhibit antidiabetic, hepatoprotective, anti-inflammatory, antioxidant, antitumor, and immune regulation activities. This review summarizes the available literature on the extraction and purification methods, structural features, biological activities, and applications of ARPS. The shortcomings of the current research and potential focus in future studies are also highlighted. This review provides systematic and current information on ARPS to promote their further exploitation and application.

KIF11 manipulates SREBP2-dependent mevalonate cross talk to promote tumor progression in pancreatic ductal adenocarcinoma.

Cholesterol metabolism is highly correlated with risks of pancreatic ductal adenocarcinoma (PDAC). Nevertheless, the underlying mechanisms of activation of cholesterol biogenesis remain inconclusive. KIF11 is a key component of the bipolar spindle and expresses highly in various malignancies. However, its functional role in PDAC tumorigenesis is still unclear. This study aims to elucidate the oncogenic functions of KIF11 in stimulating cholesterol metabolism, thereby driving PDAC progression. We utilized bioinformatics analysis to identify that KIF11 expressed highly in tumor samples versus paired normal tissues and high KIF11 correlated with high clinical stages of patients. Patients with high KIF11 had worse survival outcomes relative to those with low KIF11. Gene set enrichment analysis (GSEA) revealed that KIF11 correlated intensively with the mevalonate (MVA) metabolic pathway. Positive associations were observed between KIF11 and MVA-signature (HMGCR, FDFT1, SQLE, and MSMO1). KIF11 could elevate the free cholesterol content of PDAC cells and targeting MVA inhibited the in vitro growth of KIF11-overexpressing cells. Mechanistically, we found KIF11 could interact with SREBP2, the master regulator of MVA. High KIF11 could increase SREBP2 proteins, but not alter their mRNA levels. KIF11 could attenuate the ubiquitination-mediated degradation of SREBP2, thereby enhancing its stability and accumulation. Accordingly, KIF11 stimulated the expressions of MVA-signature and free cholesterol contents depending on SREBP2. In addition, KIF11 depended on SREBP2 to promote cell growth, migration, stemness, and colony formation abilities. The subcutaneous xenograft models indicated that targeting MVA biogenesis (atorvastatin) is effective to restrict the in vivo growth of KIF11high PDAC. Taken together, our study identified that KIF11 could activate the MVA cross talk to drive PDAC progression and inhibiting the KIF11/MVA axis provided a therapeutic vulnerability in the treatment of PDAC.

"Dual Signal-On" Split-Type Aptasensor for TNF-α: Integrating MQDs/ZIF-8@ZnO NR Arrays with MB-Liposome-Mediated Signal Amplification.

Ultrasensitive and accurate detection of biomarkers in serum is of great importance for disease diagnosis and treatment. So far, the commonly used single-mode signal suffers from certain instinct drawbacks that restrict assay performances. Herein, we report the proof-of-concept fabrication of a split-type photoelectrochemical (PEC) and electrochemical (EC) dual-modal aptasensor for ultrasensitively tracing tumor necrosis factor-α, a noteworthy biological biomarker with essential clinical importance. By smart integrating molybdenum disulfide QDs/zeolitic imidazolate framework-8@ZnO nanorod arrays with a methylene blue-liposome-mediated signal amplification strategy, "dual signal-on" detection is accomplished based on a sandwich reaction of the target with aptamer-anchored carboxyl magnetic beads and an aptamer-confined MB liposome. Linear ranges of 5 fg/mL-5 µg/mL (detection limit 1.46 fg/mL) for PEC and 10 fg/mL-0.5 µg/mL (detection limit 6.14 fg/mL) for EC are obtained, respectively. An independent signal transduction mechanism supports the accuracy improvement, and a separate biological process from a translator enables convenient fabrication, short-time consumption, wider linearity, as well as outstanding reproducibility and stability in practical application. This work presents a universal bioassay route with prospects in biomedical and related areas.

LINC01224 accelerates malignant transformation via MiR-193a-5p/CDK8 axis in gastric cancer.

BACKGROUND: Gastric cancer (GC) is a malignant tumor with a significantly high mortality rate, yet, its pathogenesis is not fully understood. Bioinformatics predicted that LINC01224 is highly expressed in stomach adenocarcinoma (STAD), and showed that LINC01224 adsorbed miR-193a-5p to target CDK8. Therefore, this study intended to verify the effect of the LINC01224/miR-193a-5p/CDK8 axis on the biological behavior of gastric cancer. METHODS: Expressions of LINC01224, miR-193a-5p, CDK8, apoptosis-, and EMT-related genes were analyzed using the GEPIA website, RT-qPCR, in situ hybridization, and Western blot as needed. Bioinformatics and dual luciferase assay were used to evaluate the relationship between LINC01224, miR-193a-5p, and CDK8. Functional experiments and rescue experiments (MTT assay, flow cytometry, wound healing assay, and Transwell) were conducted to detect the effects of the above genes on the biological characteristics of GC cells. Tumorigenesis assay was used to verify the results of in vitro experiments. RESULTS: LINC01224 adsorbed miR-193a-5p to target and upregulate CDK8. The expressions of LINC01224 and CDK8 were increased, while the expression of miR-193a-5p was decreased in GC. Overexpressed LINC01224 promoted cell viability, migration and invasion, accelerated tumor formation, attenuated apoptosis, inhibited the expressions of apoptosis-related proteins, and promoted the expressions of EMT-related proteins, whereas silenced LINC01224 led to the opposite effect. MiR-193a-5p inhibitor partially offset the effect of silenced LINC01224; interestingly, siCDK8 significantly reversed the effect of miR-193a-5p inhibitor on GC cells. CONCLUSION: LINC01224 affects the biological behavior of gastric cancer by mediating miR-193a-5p to regulate CDK8.

Development of an Autophagy Score Signature for Predicting Overall Survival in Papillary Renal Cell Carcinoma.

BACKGROUND: Autophagy is considered to be closely associated with cancer, functioning as either an anticancer or procancer mechanism depending on the cancer stage. However, the prognostic value of autophagy on papillary renal cell carcinoma (pRCC) remains unclear. In this study, our purpose was to determine the autophagy-related mRNA signature to predict the overall survival of patients with pRCC. MATERIALS AND METHODS: A total of 284 patients with pathologic confirmed pRCC in The Cancer Genome Atlas (TCGA) dataset were recruited and included. We choose patients who have smoked less than 15 years but staging 3 or 4 (including nontobacco exposure) vs. more than 15 years but staging 1 or 2. Fourteen differentially expressed mRNAs were found with fold change > 2 and P value < 0.001 through limma package after making a pair between nontobacco exposure or less than 15 years and tobacco exposure more than 15 years by matchIt package. RESULTS: Six mRNAs were identified to be significantly associated with overall survival. Then, using a risk score based on the signature of these six mRNAs, we divided the patients into low-risk and high-risk groups with significantly different OS. Further multivariate Cox regression analyses revealed that the 6-mRNA signature was independent of age, TNM stage, and tumor type. In the present study, a novel 6-mRNA signature that is useful in survival prediction in pRCC patients was developed. If validated, this mRNA signature might assist in selecting high-risk subpopulation that needs more aggressive therapeutic intervention. The risk score involved in several cancer-related pathways was identified using gene set enrichment analysis. CONCLUSION: We initially generated a six autophagy-related genes' signature, which correlates with AJCC N stage, tumor type, and pathological stage and independently predicts OS.

GC-Derived EVs Enriched with MicroRNA-675-3p Contribute to the MAPK/PD-L1-Mediated Tumor Immune Escape by Targeting CXXC4.

MicroRNAs (miRNAs) delivered by gastric cancer (GC)-secreted extracellular vesicles (GC-EVs) are associated with the immune escape in GC. Microarray analysis based on the GEO: GSE112369 dataset identified the presence of poorly expressed CXXC finger protein 4 (CXXC4) in GC, which was validated in clinical samples of GC patients. Moreover, prediction based on TargetScan analysis demonstrated the putative miR-675-3p binding site in the 3' UTR region of CXXC4. Thereby, our study aims to determine the role of GC-EV-encapsulated miR-675-3p in GC. First, CXXC4 was found to be negatively correlated with programmed cell death 1 ligand 1 (PD-L1). The effects of mitogen-activated protein kinase (MAPK) signaling on GC were evaluated using activator of the MAPK pathway. The overexpression of CXXC4 led to a downregulated MAPK signaling pathway, thus decreasing PD-L1 expression to augment the proliferation and activation of T cells co-cultured with GC HGC-27 cells. GC-EV-encapsulated miR-675-3p negatively regulated the expression of its target gene CXXC4. GC-EV-encapsulated miR-675-3p increased PD-L1 expression to stimulate the immune escape in vitro and EV-encapsulated miR-675-3p accelerated cisplatin resistance in vivo. Collectively, the aforementioned findings present a mechanism in which EV-mediated miR-675-3p upregulates PD-L1 expression, promoting immune escape in GC.

CXXC finger protein 4 inhibits the CDK18-ERK1/2 axis to suppress the immune escape of gastric cancer cells with involvement of ELK1/MIR100HG pathway.

Gastric cancer, is the fourth most common tumour type yet, ranks second in terms of the prevalence of cancer-related deaths worldwide. CXXC finger protein 4 (CXXC4) has been considered as a novel cancer suppressive factor, including gastric cancer. This study attempted to investigate the possible function of CXXC4 in gastric cancer and the underlying mechanism. The binding of the ETS domain-containing protein-1 (ELK1) to the long non-coding RNA MIR100HG promoter region was identified. Then, their expression patterns in gastric cancer tissues and cells (SGC7901) were detected. A CCK-8 assay was used to detect SGC7901 cell proliferation. Subsequently, SGC7901 cells were co-cultured with CD3+ T cells, followed by measurement of CD3+ T cell proliferation, magnitude of IFN-γ+ T cell population and IFN-γ secretion. A nude mouse model was subsequently developed for in vivo validation of the in vitro results. Low CXXC4 expression was found in SGC7901 cells. Nuclear entry of ELK1 can be inhibited by suppression of the extent of ELK1 phosphorylation. Furthermore, ELK1 is able to bind the MIR100HG promoter. Overexpression of CXXC4 resulted in weakened binding of ELK1 to the MIR100HG promoter, leading to a reduced proliferative potential of SGC7901 cells, and an increase in IFN-γ secretion from CD3+ T cells. Moreover, in vivo experiments revealed that CXXC4 inhibited immune escape of gastric cancer cells through the ERK1/2 axis. Inhibition of the CXXC4/ELK1/MIR100HG pathway suppressed the immune escape of gastric cancer cells, highlighting a possible therapeutic target for the treatment of gastric cancer.

Epidemiological and genetic characteristics of porcine reproduction and respiratory syndrome virus 2 in mainland China, 2017-2018.

Porcine reproductive and respiratory syndrome virus 2 (PRRSV2) is a major threat to the global pig industry, particularly in China, the world's largest pig-rearing and pork-production country. Continuously monitoring the epidemiological and genetic characteristics of PRRSV epidemic strains is beneficial for prevention and control of infection. Previously, we reported the epidemiological and genetic characteristics of PRRSV2 in China from 2012 to 2016. Here, the epidemiological and genetic characteristics of PRRSV2 in China from 2017 to 2018 are reported. During these two years, we collected different types of porcine samples from 2428 pig farms in 27 provinces in China. Of the 7980 samples collected, 2080 (26.07%) were positive for PRRSV2 ORF5 by RT-PCR. The positive rate of PRRSV detection between different regions of China ranged from 8.12% to 29.33%, and from 7.96% to 55.50% between different months. Phylogenetic analysis based on the ORF5 gene revealed that the PRRSV2 strains currently circulating in China belong to five clades, and most of the PRRSVs detected are highly pathogenic PRRSVs (HP-PRRSVs; clade IV) and PRRSV NADC30-like strains (clade I). Sequence analysis revealed multiple amino acid mutation types, including amino acid changes and deletions in both the GP5 and Nsp2 proteins. The presence of these mutations may have an effect on the evolution of the virus by altering the viral titer and/or affecting the antibody response against the virus.

Long non-coding RNA LSINCT5 inactivates Wnt/ß-catenin pathway to regulate MCF-7 cell proliferation and motility through targeting the miR-30a.

BACKGROUND: Breast cancer (BC) is the most common malignant tumor among women. Earlier studies showed that long stress-induced non-coding transcript 5 (LSINCT5) was implicated in BC. However, the potential mechanisms of LSINCT5 in BC is still elusive. METHODS: Relative expression of LSINCT5 in BC tissues and cells were quantified by quantitative real-time reverse transcription PCR (qRT-PCR). shRNA was employed to specifically knockdown endogenous LSINCT5 in BC cells. Cell growth and invasion activity of BC cells was assessed by colony formation and transwell migration assay, respectively. The association between LSINCT5 and miR-30a was conducted by luciferase reporter assay. Subcutaneous injection of sh-LSINCT5 transfected MCF-7 cells into the ventral regions of mice to form tumors. Mice were divided into three groups (n=10): control group, sh-NC group, sh-LSINCT5 group (sh-NC or sh-LSINCT5 transfected MCF-7 cells injected into mice). Tumor weight was checked after 30 days post-injection. RESULTS: LSINCT5 was significantly up-regulated in BC tissues and cells. LSINCT5 knockdown suppressed proliferation, invasion, and epithelial-mesenchymal transition (EMT) in vitro and in vivo. LSINCT5 acted as a sponge molecule and targeted miR-30a in BC cells. Further mechanistic study exhibited that overexpression of LSINCT5 promoted the expression of Wnt/ß-catenin-related proteins (ß-catenin, TCF4, and c-Myc). In vivo, xenograft nude mice experiment indicated sh-LSINCT5 inhibited tumor growth and motility by targeting miR-30a through modulating Wnt/ß-catenin pathway. CONCLUSIONS: The present results uncovered that LSINCT5 knockdown suppressed BC growth and metastasis via the miR-30a/Wnt/ß-catenin axis, and it served as a potential therapeutic target for early diagnosis and treatment of BC patients..

Benzethonium chloride suppresses lung cancer tumorigenesis through inducing p38-mediated cyclin D1 degradation.

Lung cancer is the leading cause of cancer-related deaths worldwide, but effective therapeutics is limited. This study aims to identify novel anticancer strategy from a Food and Drug Administration (FDA)-approved drug library consisting of 528 compounds. Benzethonium Chloride (BZN), a FDA-approved drug for anti-infective, was found to markedly induce apoptosis and inhibit proliferation and colony formation ability of lung cancer cells in dose- and time-dependent manners. BZN also enhanced the sensitivity of lung cancer cells to gefitinib, the first-line treatment strategy for selected lung cancer patients. Furthermore, BZN significantly delayed the growth of tumor xenografts in nude mice by increasing apoptosis and decreasing Ki-67 proliferation index, without obvious toxic effects to the vital organs of animals. Mechanistically, quantitative proteomics coupled with bioinformatics analyses and a series of functional assays demonstrated that BZN induced cell cycle arrest at G1 phase, and this was associated with an increase in p38-mediated phosphorylation at threonine 286 (T286) and accelerated degradation of cyclin D1. Our findings provide the first evidence that BZN could be a promising therapeutic agent in lung cancer treatment.

Iron phosphorus trichalcogenide ultrathin nanosheets: enhanced photoelectrochemical activity under visible-light irradiation.

Exploiting novel visible-light sensitive materials for the photoelectrochemical (PEC) technique is deeply meaningful for energy conversion and analytic detection. Owing to the tunable bandgap structure and strong absorption of visible light, the rising-star two-dimensional (2D) metal phosphorus trichalcogenide (MPX3) nanomaterials are expected to be promising photochemical sensitizers toward PEC biosensors. Moreover, guided by DFT calculations, the FePS3 nanosheets possessed a narrower bandgap than the bulk form, thereby enabling high availability of visible-light absorption for the FePS3 nanosheets. In this work, 2D FePS3 nanosheets were successfully synthesized by a facile salt-templated method. By tuning the proportion of the salt template, the thickness of the FePS3 nanosheets could be manipulated. As a result, the FePS3 nanosheets exhibited an obviously enhanced photoelectrochemical behavior with visible light and sensitive detection towards glucose. Being the first experimental report regarding the MPS3 nanosheets toward PEC activity, our finding can be an essential stepping stone in the pursuit of the further exploration of other 2D materials for the PEC technology.

Carbon dots-sensitized amorphous MoSx photoanode: Sequential electrodeposition preparation and dual amplified photoelectrochemical aptasensing of adenosine.

The design and fabrication of high visible-light activated photoelectrode are essential to precisely detect biomolecule in biological system. Herein, an ultrasensitive photoelectrochemical (PEC) aptasensor for specific recognition of adenosine is established based on carbon dots sensitized-amorphous molybdenum sulfide (a-MoSx/CDs) photoanode and dual amplification strategy. The heterostructured photoanode achieved by sequential electrodeposition reveals significantly boosted photocurrent with good stability and repeatability under visible light illumination, giving the credit to highly activated visible light absorption, uniform coverage and good electric contact to the underlying substrate, as well as the energy-band alignment between the two components. By stepwisely immobilizing complementary DNA probe (NH2-DNA) and adenosine aptamer (Apt), followed by methylene blue (MB) binding with the guanine base on Apt, a dual amplified self-powered PEC aptasensor for adenosine detection is constructed. Based on the co-sensitization effect of CDs and MB, ultrasensitive and high-affinitive determination of adenosine is realized over the concentration range of 0.01 nM-1000 nM at 0 V (vs. SCE), with satisfactory stability and reproducibility. The detection limit is as low as 3.3 pM, demonstrating a performance even surpassing most of the sensors reported so far. The prospective application of the co-sensitized a-MoSx photoanode for ultrasensitive aptasensing is highlighted in this work.

IL-8 is involved in radiation therapy resistance of esophageal squamous cell carcinoma via regulation of PCNA.

Esophageal squamous cell carcinoma (ESCC) is one of the prevalent and deadly cancers worldwide, especially in Eastern Asia. Our present study revealed that the expression of IL-8 was increased in radiation therapy resistance of ESCC cells. Targeted inhibition of IL-8 by its neutralization antibody (anti-IL-8) can re-sensitize ESCC cells to radiation therapy and suppress the expression of proliferating cell nuclear antigen (PCNA). IL-8 can regulate the expression of PCNA via modulating its mRNA stability and promoter activity. Mechanistically, IL-8 can regulate the expression of miR-27b-5p, which can directly bind with 3'UTR of PCNA to decrease its mRNA stability. Further, anti-IL-8 can decrease the expression of transcription factor YY1, which can bind with the promoter of PCNA to increase its transcription. Taken together, our data revealed that IL8 can regulate the radiation resistance of ESCC cells and expression of PCNA. It suggested that targeted inhibition of IL-8 may improve the clinical treatment efficiency of radio therapy.

TRIM11 promotes proliferation and glycolysis of breast cancer cells via targeting AKT/GLUT1 pathway.

Background: Tripartite motif-containing protein 11 (TRIM11) is one of the E3 ubiquitin ligases, which is upregulated in several human tumors. Meanwhile, the detailed function of TRIM11 remains unclear in breast cancer cells. Purpose: The purpose of the present study is to analyze the biological function of TRIM11 and identify its potential signaling pathway in breast cancer cells. Patients and methods: Thirty five pairs of breast cancer specimens and adjacent-matched noncancerous samples were used to analyse the expression profile of TRIM11. RNA interference was utilized to silence TRIM11 in three breast cancer cell lines (T47D, ZR7530, and BT474) respectively. Meanwhile, overexpression of TRIM11 was induced in one breast cancer cells (MDA-MB-231) by using Lentiviral vector. Moreover, the AKT inhibitor (MK-2206) was used to determine the correlation between TRIM11 and AKT in breast cancer cells. Results: Our results indicated that TRIM11 was increased in breast cancer tissues. Moreover, TRIM11 was a pro-proliferation regulator in breast cancer cells and participated in the metabolism of glycolysis. Importantly, our results demonstrated that TRIM11 was involved in the AKT/GLUT1 signaling pathway in breast cancer cells. Conclusion: Present research not only gained a deep understanding of the biological function of TRIM11 but also provided evidences to indicate its possible signaling pathway in breast cancer cells.

Overexpression of mircoRNA-137 inhibits cervical cancer cell invasion, migration and epithelial-mesenchymal transition by suppressing the TGF-ß/smad pathway via binding to GREM1.

BACKGROUND: Accumulating evidence has highlighted the tumor suppressive roles of microRNA (miRNAs) in cervical cancer (CC). In the present study, we aim to delineate the functional relevance of microRNA-137 (miR-137) in influencing epithelial-mesenchymal transition (EMT), and other CC cell biological activities via the TGF-ß/smad pathway by binding to GREM1. METHODS: Microarray analysis was initially adopted to predict the differentially expressed genes and the miRNAs related to CC, followed by the measurement of the expression patterns of GREM1, EMT-related factors in the CC tissues and the adjacent tissues. Dual luciferase reporter gene assay was conducted to determine the relationship between miR-137 and GREM1. Gain-of- and loss-of-function experiments were conducted to characterize the effects of miR-137 and GREM1 on the colony formation, proliferation, apoptosis, migration, and invasion of CC cells in vitro, and the tumorigenicity of the CC cells in nude mice. The TGF-ß/smad pathway was subsequently blocked with si-TGF-ß to investigate its involvement. RESULTS: Reduced miR-137 expression and increased GREM1 expression were predicted in CC, which was subsequently observed in the CC tissues and cells. Notably, GREM1 was a target gene of miR-137. The overexpressed miR-137 was found to inhibit EMT, cell proliferation, colony formation, invasion, migration and tumorigenesis in nude mice. In addition, miR-137 was noted to inhibit the activation of the TGF-ß/smad pathway by binding to GREM1. The silencing of TGF-ß1 was shown to reverse the effects induced by downregulated expression of miR-137. CONCLUSIONS: This study suggests that upregulated miR-137 suppresses the tumor progression in CC via blocking the TGF-ß/smad pathway by binding to and negatively regulating GREM1.

Study of suspension grafting process of polypropylene.

Grafting efficiency is an important indicator of polypropylene grafting reaction. A series of studies have been accomplished, including the conditions of free radical presence on PP backbone during peroxide initiation, the effect of preheat treatment and reaction time on PP suspension grafting results, and the effect of peroxide residue on properties of modified PP. An optimized grafting process was proposed by mixing and preheating polypropylene (PP) and the initiator benzoyl peroxide (BPO) before adding the grafting monomer glycidyl methacrylate (GMA),resulting in an increase in grafting efficiency from 50.0% to 78.2%. With initiator residue removed by alternating temperature treatment, the suspension grafting reaction time could be substantially reduced.

VS2 quantum dot label-free fluorescent probe for sensitive and selective detection of ALP.

As an essential enzyme highly associated with various human diseases, alkaline phosphatase (ALP) plays an important role in human tissues. Developing new materials and strategies for monitoring ALP is thus important. We have developed a novel label-free fluorescent sensing system for ALP activity that is based on the "turn-on" fluorescence of VS2 quantum dots. The fluorescence of VS2 quantum dots quenched by Fe3+ can be restored by ascorbic acid, which is generated by hydrolysis of L-ascorbic acid 2-phosphate catalyzed by ALP. Rapid, convenient, and sensitive detection of ALP is achieved in the range from 3 to 1000 U/L (R 2 =0.9985), with a detection limit of 0.27 U/L. The proposed sensor exhibits excellent selectivity for ALP compared with other enzymes and proteins, such as glucose oxidase, lysozyme, trypsin, human serum albumin, and bovine serum albumin. The reliability for ALP determination in human serum plasma has been demonstrated with satisfactory recovery, revealing promising application in clinical diagnosis and biomedical research. Graphical abstract Hydrothermally synthesized VS2 quantum dots serving as a novel turn-on fluorescent probe for detection of alkaline phosphatase (ALP) activity. AA L-ascorbic acid, AAP L-ascorbic acid 2-phosphate, NAC N-acetyl-L-cysteine.