Research on the construction of a collaborative ability evaluation system for the joint graduation design of new engineering specialty groups based on digital technology.

Conducting research on the construction of a collaborative ability evaluation system for the joint graduation design of new engineering specialty groups based on digital technology holds great practical relevance. In this paper, which is based on a comprehensive analysis and research of the current situation pertaining to the joint graduation design of college graduates in China and elsewhere and on the construction of a collaborative ability evaluation system, combined with the talent training program of the joint graduation design, the Delphi method and the analytic hierarchy process (AHP) are adopted to establish a hierarchical structure model of the collaborative ability evaluation system for joint graduation design. In this system, collaborative abilities in the areas of cognition, behavior and emergency management are used as the criteria level evaluation indices. Additionally, collaborative ability in regard to targets, to knowledge, to relationships, to software, to the workflow, to organization, to culture, to learning and to conflict are used as evaluation indices. The comparison judgment matrix of the evaluation indices is constructed at the collaborative ability criterion level and at the index level. By calculating the maximum eigenvalue and corresponding eigenvector of the judgment matrix, the weight assignment of the evaluation indices is obtained, and the evaluation indices are sorted. Finally, the related research content is evaluated. The research results show that the key evaluation indicators for the collaborative ability evaluation system of joint graduation design that need to be considered are easy to determine, and these indicators provide a theoretical reference for the reform of graduation design teaching of new engineering specialty groups.

Long noncoding RNA HULC regulates the NF-κB pathway and represents a promising prognostic biomarker in liver cancer.

BACKGROUND: Long noncoding RNAs (lncRNAs) are involved in a diverse array of biological processes. While lncRNAs are commonly upregulated in hepatocellular carcinoma (HCC), the specific regulatory roles they play in this oncogenic context require further study and clarification. Although HULC (lncRNA highly upregulated in liver cancer) is involved in disease pathogenesis, its precise role in this context remains unclear. METHODS: Here, we have explored the mechanistic relevance of HULC expression by assessing its expression in patient samples. The importance of this lncRNA in the onset and progression of HCC was investigated through in vitro approaches including Western blotting, quantitative PCR, Transwell assays, electron microscopy, wound healing assays, and real-time cell analysis (RTCA). Additionally, the in vivo functions of this lncRNA were assessed using an orthotopic HCC xenograft in nude mouse model system. RESULTS: HULC was identified as a lncRNA that is highly upregulated in human liver tumors. In vitro, HULC was able to promote HCC malignancy, although its excess overexpression also led robust autophagic induction, promoting the increased expression of autophagy-associated genes including LC3 and Beclin-1. At a mechanistic level, HULC was able to promote the phosphorylation of p65 and IkBkB thus enhancing autophagy by increasing LC3II levels in a manner dependent upon the NF-κB pathway. HULC downregulation was also linked to impaired orthotopic HCC tumor growth in vivo. The link between HULC and autophagy may play a role in disease progression. CONCLUSIONS: These results suggest that HULC is an oncogenic lncRNA, and may thus offer value as a prognostic biomarker and promoter of HCC development, in addition to being a potential therapeutic target in this cancer type.

Compound 78c exerts a therapeutic effect on collagen-induced arthritis and rheumatoid arthritis.

OBJECTIVES: Many studies have found that CD38 expression is increased in rheumatoid arthritis (RA), an autoimmune disease in which immune tolerance is dysregulated. Inhibition of CD38 expression or activity can significantly alleviate collagen-induced arthritis (CIA), a well-known animal model used for the study of RA. This study aimed to confirm the therapeutic effect of 78c, a specific inhibitor of CD38, and the role of CD38+ NK cells in immune imbalance in RA. METHODS: CIA mice were injected with 78c to observe the therapeutic effect. CD38+ NK cells were extracted from human peripheral blood and treated with 78c. The pretreated NK cells were co-cultured with CD4+ T cells. RESULTS: We found that 78c significantly suppressed joint inflammation; reduced the levels of B cells, IL-6 and TNF-α; and increased the levels of IL-10, energy metabolism and spontaneous movement in CIA mice. 78c treatment also increased Treg cell numbers and decreased the Th1/Th2 ratio in the CIA model animals. Moreover, the proportion of CD38+ NK cells was increased in the CIA mice and significantly decreased following 78c treatment. Human CD4+ T cells that were co-cultured with 78c-pretreated CD38+ NK cells differentiated into more Treg cells and had lower Th17/Treg and Th1/Th2 ratios than CD4+ T cells co-cultured with CD38+ NK cells without the pretreatment. Transcriptomic analyses demonstrated that 78c changed expression pro les in CD38+ NK cells. CONCLUSIONS: These results suggested that 78c could be used for the treatment of RA and CIA as it alleviates the inhibitory effect of CD38+ NK cells on CD4+ T cell differentiation to Treg cells to restore immune balance.

Identification and validation of the N6-methyladenosine RNA methylation regulator ZC3H13 as a novel prognostic marker and potential target for hepatocellular carcinoma.

N6-methyladenosine (m6A) RNA methylation has been implicated in various malignancies. This study aimed to identify prognostic signature based on m6A methylation regulators for hepatocellular carcinoma (HCC) and provide candidate targets for HCC treatment. In this study, the expression levels, prognostic values, correlation with tumor grades and genetic variations of m6A-related genes in HCC were evaluated using bioinformatics analyses. Interestingly, the results show that methyltransferase zinc finger CCCH-type containing 13 (ZC3H13) was expressed at a significantly low level in HCC. Survival outcome analysis suggested that significant correlations existed between ZC3H13 downregulation and poor overall survival (OS) and poor recurrence-free survival (RFS) in HCC patients. Therefore, ZC3H13 was chosen for further experimental validation. The expression of ZC3H13 in HCC cell lines was investigated by western blotting. Knockdown of ZC3H13 significantly enhanced the migration and invasion of HCC cells, as demonstrated by wound healing and transwell assays. Moreover, upregulating ZC3H13 repressed the growth of xenograft tumors in vivo. Functional and pathway enrichment analyses indicated that ZC3H13 might be involved in transcriptional dysregulation or the JAK-STAT signaling pathway in cancer. Additionally, ZC3H13 expression was significantly correlated with lymphocytes and immunomodulators. Therefore, ZC3H13 is a promising candidate as a novel biomarker and therapeutic target for HCC.

Poly-adenine-mediated spherical nucleic acid probes for live cell fluorescence imaging of tumor-related microRNAs.

BACKGROUND: Accurately detecting and quantifying tumor-related microRNAs (miRNAs) in living cells is of great value for early cancer diagnosis. Herein, we present poly-adenine (polyA)-mediated spherical nucleic acid (SNA) nanoprobes for intracellular miRNA imaging in living cells. METHODS AND RESULTS: polyA-mediated spherical nucleic acid (pASNA) nanoprobes consist of gold nanoparticles (AuNPs) anchored with fluorophore-labeled DNA molecules pre-hybridized with recognition sequences and polyA tails. The detection performance for miRNAs in vitro was studied to confirm the feasibility of pASNA nanoprobes for imaging live cell miRNAs. Before the pASNA nanoprobes were used for imaging intracellular miRNAs in MCF-7, HeLa, and LO2 cells, the stability and non-cytotoxicity were investigated using Dnase I and a standard colorimetric CCK8 assay. Flow cytometry, qRT-PCR analyses were conducted to confirm the different expression levels of miR-155 in live cells. Results showed that the pASNA nanoprobes had good detection sensitivity and specificity, excellent stability, and low toxicity. After incubating with pASNA nanoprobes, noticeable fluorescence signal enhancement could be clearly observed in MCF-7 and HeLa cells but not LO2 cells by confocal microscopy. Flow cytometry analysis and qRT-PCR indicated that MCF-7 and HeLa cells had higher miR-155 expression levels compared to LO2 cells. CONCLUSIONS: The pASNA nanoprobes we developed had good sensitivity and specificity, excellent nuclease stability and low toxicity, thus representing a new approach to exquisitely reveal the distribution of endogenous miRNAs in live cells.

Chorionic villus-derived mesenchymal stem cell-mediated autophagy promotes the proliferation and invasiveness of trophoblasts under hypoxia by activating the JAK2/STAT3 signalling pathway.

BACKGROUND: Trophoblast dysfunction during pregnancy is fundamentally involved in preeclampsia. Several studies have revealed that human chorionic villous mesenchymal stem cells (CV-MSCs) could regulate trophoblasts function. RESULTS: To understand how human chorionic villous mesenchymal stem cells (CV-MSCs) regulate trophoblast function, we treated trophoblasts with CV-MSC supernatant under hypoxic conditions. Treatment markedly enhanced proliferation and invasion and augmented autophagy. Transcriptome and pathway analyses of trophoblasts before and after treatment revealed JAK2/STAT3 signalling as an upstream regulator. In addition, STAT3 mRNA and protein levels increased during CV-MSC treatment. Consistent with these findings, JAK2/STAT3 signalling inhibition reduced the autophagy, survival and invasion of trophoblasts, even in the presence of CV-MSCs, and blocking autophagy did not affect STAT3 activation in trophoblasts treated with CV-MSCs. Importantly, STAT3 overexpression increased autophagy levels in trophoblasts; thus, it positively regulated autophagy in hypoxic trophoblasts. Human placental explants also proved our findings by showing that STAT3 was activated and that LC3B-II levels were increased by CV-MSC treatment. CONCLUSION: In summary, our data suggest that CV-MSC-dependent JAK2/STAT3 signalling activation is a prerequisite for autophagy upregulation in trophoblasts.

N-Myc promotes angiogenesis and therapeutic resistance of prostate cancer by TEM8.

Although patients with early localized prostate cancer can survive longer, castration-resistant prostate cancer (CRPC) has gradually emerged with the use of androgen deprivation therapy (ADT). N-Myc and TEM8 play a vital role in the progression of several cancer types. However, the underlying mechanism of how N-Myc and TEM8 promote the progression of prostate cancer remains unclear. In this study, the expression of N-Myc and TEM8 was detected in benign prostatic hyperplasia (BPH) and prostate cancer (PCa) tissues by immunohistochemistry (IHC). LNCaP cell lines were maintained in RPMI 1640 medium supplemented with 10% charcoal-stripped fetal bovine serum. Subsequently, R language software was used to verify our results. Tubule formation assay of human umbilical vein endothelial cell (HUVEC) was conducted to examine the effect of N-Myc and TEM8 overexpression on angiogenesis in prostate cancer cells. IHC results showed a positive correlation between the expression of N-Myc and TEM8 in prostate cancer tissues. Further analysis showed that N-Myc and TEM8 were associated with clinicopathological features and poor prognosis in prostate cancer patients. Moreover, the overexpression of N-Myc and TEM8 promoted proliferation of prostate cancer cells and angiogenesis. Additionally, N-Myc and TEM8 overexpression was associated with therapeutic resistance. We further found that N-Myc promoted angiogenesis and therapeutic resistance in prostate cancer via TEM8. Hence, targeting N-Myc/TEM8 pathway in prostate cancer would be a novel therapeutic strategy to enhance the treatment of prostate cancer patients.

DNA tetrahedron-mediated immune-sandwich assay for rapid and sensitive detection of PSA through a microfluidic electrochemical detection system.

Prostate-specific antigen (PSA) is the most widely used biomarker for the early diagnosis of prostate cancer. Existing methods for PSA detection are burdened with some limitations and require improvement. Herein, we developed a novel microfluidic-electrochemical (µFEC) detection system for PSA detection. First, we constructed an electrochemical biosensor based on screen-printed electrodes (SPEs) with modification of gold nanoflowers (Au NFs) and DNA tetrahedron structural probes (TSPs), which showed great detection performance. Second, we fabricated microfluidic chips by DNA TSP-Au NF-modified SPEs and a PDMS layer with designed dense meandering microchannels. Finally, the µFEC detection system was achieved based on microfluidic chips integrated with the liquid automatic conveying unit and electrochemical detection platform. The µFEC system we developed acquired great detection performance for PSA detection in PBS solution. For PSA assays in spiked serum samples of the µFEC system, we obtained a linear dynamic range of 1-100 ng/mL with a limit of detection of 0.2 ng/mL and a total reaction time <25 min. Real serum samples of prostate cancer patients presented a strong correlation between the "gold-standard" chemiluminescence assays and the µFEC system. In terms of operation procedure, cost, and reaction time, our method was superior to the current methods for PSA detection and shows great potential for practical clinical application in the future.

Optimizing the system-wide layout of sewage treatment plants based on enumeration and the orthogonal test.

Optimizing the locations of sewage treatment plants has enormous practical significance. In this study, a large-system mathematical model was developed for optimizing the locations of sewage treatment plants within a system and designing the associated pumping station pipe network. Head loss of pipe segments in the pipe network was the coupling constraint, the economic flow rate of pipe segments was determined by the feasible region constraints of decision variables, and the design variables were the sewage treatment plant locations, the design head of the pumping stations, the pipeline economic life, and the pipe diameter of divided pipe segments. The minimum total annual cost of the sewage treatment plant(s) and the pumping station pipe network was the objective function. A large-system quadratic orthogonal test-based selection method was used with a discrete enumeration comparison and selection method to determine pipeline economic life. A dynamic programming method was used to determine the pipe diameter of the divided pipe segments. By comparing the total annual cost of the sewage treatment plants and the associated pumping station pipe network corresponding to different pipeline economic lifetimes, the optimal solution that generates the minimum total annual cost can be identified. The sewage treatment plant and pumping station pipe network in Taizhou, China, was used as an example to compare and analyze optimization results. The new optimization method would have produced much lower annual cost than that of the existing system. This study provides valuable theoretical references for probing the layout design of urban sewage treatment plants corresponding to different pipeline economic lifetimes.

TRAIL promotes hepatocellular carcinoma apoptosis and inhibits proliferation and migration via interacting with IER3.

Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) can induce substantial cytotoxicity in tumor cells but rarely exert cytotoxic activity on non-transformed cells. In the present study, we therefore evaluated interactions between TRAIL and IER3 via co-immunoprecipitation and immunofluorescence analyses, leading us to determine that these two proteins were able to drive the apoptotic death of hepatocellular carcinoma (HCC) cells and to disrupt their proliferative and migratory abilities both in vitro and in vivo. From a mechanistic perspective, we determined that TRAIL and IER3 were capable of inhibiting Wnt/ß-catenin signaling. Together, these results indicate that TRAIL can control the pathogenesis of HCC at least in part via interacting with IER3 to inhibit Wnt/ß-catenin signaling, thus indicating that this TRAIL/IER3/ß-catenin axis may be a viable therapeutic target in HCC patients.

MiR-148b-3p Regulates the Expression of DTYMK to Drive Hepatocellular Carcinoma Cell Proliferation and Metastasis.

Deoxythymidilate kinase (DTYMK) has been identified as a putative oncogene associated with the incidence of hepatocellular carcinoma (HCC), but the mechanisms whereby it regulates this cancer type remain uncertain. The present study was therefore designed to explore the role of DTYMK in HCC and to evaluate the underlying molecular mechanisms. MiRNAs associated with DTYMK expression levels in HCC were identified through analyses of both clinical samples and publically available gene expression datasets. We then assessed the putative functions of DTYMK and miR-148b-3p in this oncogenic context through studies of HCC cells and a murine xenograft model system. Correlation analyses and in vitro experiments led us to confirm DTYMK as a target of miR-148b-3p. In addition, we assessed dTTP levels associated with the DTYMK pathway in HCC cells to understand the functional implications of our experimental findings. We found that HCC tissues and cells exhibited marked DTYMK upregulation and miR-148b-3p downregulation, with the expression levels of DTYMK and miR-148b-3p being negatively correlated with one another. The impact of overexpressing DTYMK in tumor cells was partially reversed upon cellular transfection with miR-148b-3p mimics, providing conclusive evidence that DTMYK is a target of this miRNA. Importantly, DTYMK-related dTTP levels were also impacted by miR-148b-3p mimic transfection. DTYMK is a key regulator of HCC progression, and its expression is suppressed by miR-148b-3p, suggesting that this miR-148b-3p/DTYMK regulatory axis may be amenable to therapeutic targeting in patients with HCC.

N­Myc induces the tumor progression of prostate cancer by regulating FSCN1.

The oncoprotein N­Myc has a carcinogenic effect in numerous types of cancer, and it can cause castration resistance in prostate cancer (PCa), and leads to the development of small cell neuroendocrine cancer by regulating multiple target genes. Immunohistochemical staining, RT­qPCR, western blotting, wound healing and CCK­8 assays were used to detect the expression of N­Myc and FSCN1 as well as AR and CgA at the human level and cell level. The immunohistochemical results revealed that the protein levels of N­Myc proto­oncogene protein (N­Myc) and fascin (FSCN1) in PCa were significantly higher than that of hyperplastic tissues (P<0.05), and there was a weak correlation between them (P=0.002). In vitro, N­Myc and FSCN1 were overexpressed in LNCaP and C4­2 cell lines. The results revealed the promoting effect of N­Myc and FSCN1 on malignant progression of PCa. In addition, the endogenous FSCN1 was knocked down in the C4­2 cell line, and the results revealed that the silencing of FSCN1 enhanced the expression of N­Myc and weakened the expression of the neuroendocrine marker CgA. Therefore, the present findings indicated that N­Myc may promote the malignant process of PCa by regulating FSCN1 and FSCN1 may have a reverse regulatory effect on N­Myc.

Dermatopontin inhibits WNT signaling pathway via CXXC finger protein 4 in hepatocellular carcinoma.

Hepatocellular carcinoma (HCC) is a major cause of tumor associated deaths globally. Annually, the prevalence of HCC is increasing and the lack of early prognostic indicators manifests a dismal prognosis for HCC patients. A deep understanding of the molecular events that promote HCC progression are required for the design of new diagnostics and therapeutics. Dermatopontin (DPT) is an extracellular matrix protein that regulates the metastatic phenotypes of many cancers. However, the effects of DPT on HCC cell growth remain undefined. In this study, we demonstrate that the exogenous expression of DPT inhibits HCC cell growth both in vitro and in vivo. Furthermore, we show that DPT regulates CXXC4, which in turn targets c-Myc, EZH2, SOX2 and ß-catenin, through its ability to impact Wnt signaling pathway. These data suggest that DPT regulates CXXC4, c-Myc, EZH2, SOX2 and ß-catenin, through Wnt signaling to repress HCC proliferation. This highlights DPT as promising target for future HCC diagnostics and therapeutic targets.

Electrochemical DNA Sensor for Sensitive BRCA1 Detection Based on DNA Tetrahedral-Structured Probe and Poly-Adenine Mediated Gold Nanoparticles.

BRCA1 is the biomarker for the early diagnosis of breast cancer. Detection of BRCA1 has great significance for the genetic analysis, early diagnosis and clinical treatment of breast cancer. In this work, we developed a simple electrochemical DNA sensor based on a DNA tetrahedral-structured probe (TSP) and poly-adenine (polyA) mediated gold nanoparticles (AuNPs) for the sensitive detection of BRCA1. A thiol-modified TSP was used as the scaffold on the surface of the screen-printed AuNPs electrode. The capture DNA (TSP) and reporter DNA were hybridized to the target DNA (BRCA1), respectively, to form the typical sandwich system. The nanocomposites of reporter DNA (polyA at the 5' end) combined with AuNPs were employed for signal amplification which can capture multiple enzymes by the specificity between biotin and streptavidin. Measurements were completed in the electrochemical workstation by cyclic voltammetry and amperometry and we obtained the low limit of detection of 0.1 fM with the linear range from 1 fM to 1 nM. High sensitivity and good specificity of the proposed electrochemical DNA sensor showed potential applications in clinical early diagnosis for breast cancer.

Optimization design method for urban sewage collection pipe networks.

In this study, a secondary subsystem mathematical model is established under the condition that the layout of the sewage collection branch, trunk, and main pipe network projects is fixed. The sewage collection branch and trunk pipe network projects are treated as the research objective by taking the minimum annual cost of the sewage collection pipe network projects as the objective function, the longitudinal slope of the pipe section and the economic flow rate of the pipe section as constraints, and the diameter of the pipe section as the decision variable. A first-level subsystem mathematical model is established by taking the sewage collection branch, trunk, and main pipe network project as the research object. A large system mathematical model is established in the same manner. This model can be solved using the large system secondary decomposition-dynamic programming aggregation method, and the optimal diameter for each pipe section can be obtained. A regional sewage collection pipe network project in Taizhou city was considered as an example for comparative analysis before and after optimization, and the results verified that the optimization method proposed in this study can solve this complex large system optimization problem.

TUG1 long non-coding RNA enlists the USF1 transcription factor to overexpress ROMO1 leading to hepatocellular carcinoma growth and metastasis.

Hepatocellular carcinoma (HCC) is a prevalent and highly aggressive cancer. Long non-coding RNAs (lncRNAs) are recognized as potential molecular targets for HCC and are currently under increased research focus. Here, we investigate the regulatory processes underlying the axis of the lncRNA taurine upregulated gene 1 (TUG1), Upstream Transcription Factor 1 (USF1), and reactive oxygen species modulator 1 (ROMO1) in the propagation and metastasis of HCC cells. Distribution of lncRNA TUG1 was found to be prominent in HCC cell cytoplasm and nuclei. LncRNA TUG1 conscripted the USF1 transcription factor to enhance the promoter function of ROMO1. Enlisting the USF1 transcription factor to increase ROMO1 expression following upregulation of TUG1 lncRNA enhanced HCC Huh7 cell proliferation, motility, and metastasis. Rapid tumor proliferation in nude mice provided in vivo verification. The importance of the lncRNA TUG1/USF1/ROMO1 complex as a target for HCC therapy is a key result of this investigation which is exemplified by its role in regulating the proliferation, motility, and metastasis of HCC cells.

LncRNA MALAT1 acts as a miR-125a-3p sponge to regulate FOXM1 expression and promote hepatocellular carcinoma progression.

Background: Hepatocellular carcinoma (HCC) is a prominent cancer type, with long non-coding RNAs (lncRNAs) being known to be relevant to its progression. We therefore investigated how a particular lncRNA known as the metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) was associated with HCC. Methods: Quantitative reverse transcriptase PCR (qPCR) was used to assess expression of MALAT1, Forkhead Box M1 (FOXM1) and miR-125a-3p in HCC tissue samples. How MALAT1 regulates HCC proliferation and metastasis was assessed through appropriate assays. FOXM1 was identified as a miR-125a-3p target using luciferase assays, and how MALAT1/miR-125a-3p alter FOXM1 expression was explored via qPCR and Western blotting. Results: HCC tissues exhibited MALAT1 upregulation. miR-125a-3p targeted FOXM1 and could be regulated by MALAT1. MALAT1 knockdown disrupted proliferation and invasion, whereas miR-125a-3p knockdown partially reversed this phenotype. Conclusions: These results indicate that MALAT1 modulates FOXM1 expression via being a miR-125a-3p sponge, thus promoting HCC progression.

Effects of Notch Signaling Pathway in Cervical Cancer by Curcumin Mediated Photodynamic Therapy and Its Possible Mechanisms in Vitro and in Vivo.

Curcumin, as a high effect and low toxicity anti-cancer drug and photosensitiser, has synergistic and complementary effects with photodynamic therapy (PDT). However, due to its unclear mechanism, PDT's application and efficacy were limited. Notch signaling pathway, which is highly correlates with carcinogenesis and development of cervical cancer, could be a potential therapeutic targets to improve the effectiveness of PDT. Therefore, in this study, we explored the effects of Notch signaling pathway in cervical cancer by curcumin mediated PDT with/without Notch receptor blocker (DAPT), and hope to elucidate its mechanism. Firstly, the effect on the proliferation of cervical cancer Me180 cells were detected with MTT assay, and apoptosis were detected with Annexin V-FITC/PI combined with flow cytometry. Secondly, after establishment of nude mice model, dividing the experimental animals into model group, curcumin PDT group, simple DAPT group, and curcumin-PDT+DAPT group, and analyzing tumor volume changes as well as HE staining in each group. mRNA and protein expression of gene Notch-1 and its downstream NF-κB and VEGF were observed with RT-PCR, immunohistochemical staining and Western-blot with/without inhibition of Notch signaling pathway by DAPT, both in vivo and in vitro experiments. We found both DAPT and curcumin-PDT can inhibit the proliferation and induce apoptosis of cervical cancer cell. The two have synergistic effect in vitro and in vivo. This effect can effectively block the conduction of Notch signaling pathway, which is associated with down-regulation of the expression of Notch1 and NF-κB. Notch signaling pathway could be one of the targets of curcumin-PDT photodynamic therapy.

Framework Nucleic Acid-Enabled Programming of Electrochemical Catalytic Properties of Artificial Enzymes.

The creation and engineering of artificial enzymes remain a challenge, especially the arrangement of enzymes into geometric patterns with nanometer precision. In this work, we fabricated a series of novel DNA-tetrahedron-scaffolded-DNAzymes (Tetrazymes) and evaluated the catalytic activity of these Tetrazymes by electrochemistry. Tetrazymes were constructed by precisely positioning G-quadruplex on different sites of a DNA tetrahedral framework, with hemin employed as the co-catalyst. Immobilization of Tetrazymes on a gold electrode surface revealed horseradish peroxidase (HPR)-mimicking bioelectrocatalytic property. Cyclic voltammogram and amperometry were employed to evaluate the capability of Tetrazymes of different configurations to electrocatalyze the reduction of hydrogen peroxide (H2O2). These artificial Tetrazymes displayed 6- to 14-fold higher enzymatic activity than G-quadruplex/hemin (G4-hemin) without the DNA tetrahedron scaffold, demonstrating application potential in developing novel G-quadruplex-based electrochemical sensors.

MALAT1 promotes angiogenesis of breast cancer.

Metastasis­associated lung adenocarcinoma transcript 1 (MALAT1) is a long non­coding RNA (lncRNA) that has an oncogenic role in some types of cancers, uncluding breast cancer (BC). To investigate the role of MALAT1 in human BC progression, we detected MALAT1 expression levels based on tissue samples from 20 BC cases and 20 healthy controls and found MALAT1 expression levels to be significantly high (P<0.05). Then, we knocked down endogenous MALAT1 in MCF­7 cells using MALAT1 short hairpin RNA (shRNA). The results revealed that MALAT1 knockdown could significantly inhibit proliferation, migration, and tube formation in vitro. In addition, miR­145 expression inversely changed in BC tissue cases. Furthermore, knockdown of endogenous MALAT1 significantly increased miR­145 levels in MCF­7 cells. This finding indicated an interaction between MALAT1 and miR­145. In addition, knockdown of MALAT1 significantly reduced the expression of vascular endothelial growth factor in MCF­7 cells. This outcome revealed that MALAT1 promoted angiogenesis in BC, which may be related to the expression of miR­145.