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With the increase of wastewater discharge, the requirement of wastewater treatment technology is gradually increased. How to treat wastewater economically, while making the treatment process short, easy to manage and low running cost, is the focus of attention. Adsorption-biological coupling technology could make adsorption and biodegradation complement each other, which has coupled accumulation effect. In this study, with coke as the adsorbent, the efficiency of the adsorption-biological coupling reactor on the treatment of total phosphorus (TP), chemical oxygen demand (COD), and ammonia nitrogen (NH

BRAF is frequently mutated in various cancer types and contributes to tumorigenesis and metastasis. As an important switch in RAS signalling pathway, BRAF typically enables the activation of MEK and ERK, and its mutation significantly promotes metastasis. However, whether BRAF could stimulate metastasis in a MEK/ERK signalling-independent manner is still unknown. Herein, we found that a portion of the BRAF protein localized at the plasma membrane and that the BRAFV600E mutation led to abundant formation of filopodia, which is a hallmark of invasive cancer cells. Mechanistically, BRAF physically interacts with the pseudopod formation-related protein Vasodilator-stimulated phosphoprotein (VASP), and BRAF specifically catalyzes VASP phosphorylation at Ser157. VASP depletion or disruption of Ser157 phosphorylation preferentially reduced the motility, invasion and metastasis of tumor cells harboring oncogenic BRAF or KRAS. Moreover, in clinical cancer tissues, BRAFV600E was positively correlated with the extent of invasion, and tissues with BRAFV600E expression exhibited elevated levels of VASP Ser157 phosphorylation. Our study therefor reveals a noncanonical mechanism by which oncogenic BRAF or KRAS promotes metastasis, suggests that VASP Ser157 phosphorylation might serve as a valuable therapeutic target in BRAF or KRAS mutant cancers.

Diabetic osteoporosis is secondary osteoporosis and a serious complication of diabetes with a high incidence rate and poor prognosis. The specific mechanism of diabetic osteoporosis is unclear, and prevention and treatment options are limited. Recently, melatonin has been found to prevent and treat diabetic osteoporosis. Herein, we investigated the mechanism whereby melatonin inhibits osteoclastogenesis and identified a new target for osteoporosis treatment. We established an in vitro osteoblast-osteoclast co-culture system as a diabetic osteoporosis model. Osteoclastogenesis was determined using tartrate-resistant acid phosphatase staining and cathepsin K expression. Real-time PCR was used to ascertain expression of microRNA mir-882, targeting Rev-Erbα. Western blotting was performed to detect the expression of Rev-Erbα, receptor activator of NF-kB ligand (RANKL), and osteoprotegerin (OPG), and ELISA was utilized to analyse the secreted form of RANKL. High glucose promoted osteoclastogenesis and elevated the RANKL/OPG ratio in osteoblasts, while melatonin reversed these effects. High glucose inhibited Rev-Erbα expression, while melatonin promoted its expression. Conversely, high glucose promoted mir-882 expression, while melatonin inhibited it. We infer that melatonin inhibits RANKL expression in osteoblasts via the mir-882/Rev-Erbα axis, thus inhibiting osteoclastogenesis. Our findings provide insights into diabetic osteoporosis and identify a new therapeutic target for osteoporosis.

Exogenous melatonin inhibited the senescence of preosteoblast cells in type 1 diabetic (T1D) mice and those cultured in high glucose (HG) by multiple regulations. Exogenous melatonin had a protective effect on diabetic osteoporosis, which may depend on the inhibition of senescence. Senescence is thought to play an important role in the pathophysiological mechanisms underlying diabetic bone loss. Increasing evidence has shown that melatonin exerts anti-senescence effects. In this study, we investigated whether melatonin can inhibit senescence and prevent diabetic bone loss. C57BL/6 mice received a single intraperitoneal injection of 160 mg/kg streptozotocin, followed by the oral administration of melatonin or vehicle for 2 months. Then, tissues were harvested and subsequently examined. MC3T3-E1 cells were cultured under HG conditions for 7 days and then treated with melatonin or not for 24 h. Sirt1-specific siRNAs and MT1- or MT2-specific shRNA plasmids were transfected into MC3T3-E1 cells for mechanistic study. The total protein extracted from mouse femurs revealed that melatonin prevented senescence in T1D mice. The micro-CT results indicated that melatonin prevented bone loss in T1D mice. Cellular experiments indicated that melatonin administration prevented HG-induced senescence, whereas knockdown of the melatonin receptors MT1 or MT2 abolished these effects. Sirt1 expression was upregulated by melatonin administration but significantly reduced after MT1 or MT2 was knocked down. Knockdown of Sirt1 blocked the anti-senescence effects of melatonin. Additionally, melatonin promoted the expression of CDK2, CDK4, and CyclinD1, while knockdown of MT1 or MT2 abolished these effects. Furthermore, melatonin increased the expression of the polycomb repressive complex (PRC), but knockdown of MT1 or MT2 abolished these effects. Furthermore, melatonin increased the protein levels of Sirt1, PRC1/2 complex–, and cell cycle–related proteins. This work shows that melatonin protects against T1D-induced bone loss, probably by inhibiting senescence. Targeting senescence in the investigation of diabetic osteoporosis may lead to novel discoveries.

Melatonin, secreted in a typical diurnal rhythm pattern, has been reported to prevent osteoporosis; however, its role in osteoclastogenesis remains unclear. In the present study, the ability of melatonin to inhibit receptor activator of nuclear factor‑κB ligand (RANKL)‑induced osteoclastogenesis and the associated mechanism were investigated. Raw264.7 cells were cultured with RANKL (100 ng/ml) and macrophage colony‑stimulating factor (M‑CSF; 30 ng/ml) for 7 days, and tartrate‑resistant acid phosphatase (TRAP) staining was used to detect osteoclastogenesis following treatment with melatonin. In addition, the effect of melatonin on cathepsin K and microRNA (miR)‑882 expression was investigated via western blotting and reverse transcription‑quantitative PCR. Melatonin significantly inhibited RANKL‑induced osteoclastogenesis in Raw264.7 cells. From bioinformatics analysis, it was inferred that nuclear receptor subfamily 1 group D member 1 (NR1D1/Rev‑erbα) may be a target of miR‑882. In vitro, melatonin upregulated Rev‑erbα expression and downregulated miR‑882 expression in the osteoclastogenesis model. Rev‑erbα overexpression boosted the anti‑osteoclastogenesis effects of melatonin, whereas miR‑882 partially diminished these effects. The present results indicated that the miR‑882/Rev‑erbα axis may serve a vital role in inhibiting osteoclastogenesis following RANKL and M‑CSF treatment, indicating that Rev‑erbα agonism or miR‑882 inhibition may represent mechanisms through which melatonin prevents osteoporosis.

Background Deregulated circular RNAs (circRNAs) are associated with the development of cancer and therapy resistance. However, functional research of circRNAs mostly focus on potential miRNA or protein binding and more potential regulation of circRNA on host gene DNA in cancers are yet to be inspected. Method We performed total RNA sequencing on clinical breast cancer samples and identified the expression patterns of circRNAs and corresponding host genes in patient blood, tumor and adjacent normal tissues. qPCR, northern blot and in situ hybridization were used to validate the dysregulation of circRNA circSMARCA5. A series of procedures including R-loop dot-blotting, DNA-RNA immunoprecipitation and mass spectrum, etc. were conducted to explore the regulation of circSMARCA5 on the transcription of exon 15 of SMARCA5. Moreover, immunofluorescence and in vivo experiments were executed to investigate the overexpression of circSMARCA5 with drug sensitivities. Results We found that circRNAs has average higher expression over its host linear genes in peripheral blood. Compared to adjacent normal tissues, circSMARCA5 is decreased in breast cancer tissues, contrary to host gene SMARCA5. The enforced expression of circSMARCA5 induced drug sensitivity of breast cancer cell lines in vitro and in vivo. Furthermore, we demonstrated that circSMARCA5 can bind to its parent gene locus, forming an R-loop, which results in transcriptional pausing at exon 15 of SMARCA5. CircSMARCA5 expression resulted in the downregulation of SMARCA5 and the production of a truncated nonfunctional protein, and the overexpression of circSMARCA5 was sufficient to improve sensitivity to cytotoxic drugs. Conclusion Our results revealed a new regulatory mechanism for circRNA on its host gene and provided evidence that circSMARCA5 may serve as a therapeutic target for drug-resistant breast cancer patients.

Previous studies have demonstrated that the antitumor potential of IU1 (a pharmacological compound), which was mediated by selective inhibition of proteasome-associated deubiquitinase ubiquitin-specific protease 14 (USP14). However, the underlying molecular mechanisms remain elusive. It has been well established that mdm2 (Murine double minute 2) gene was amplified and/or overexpressed in a variety of human neoplasms, including cervical cancer. Furthermore, MDM2 is critical to cervical cancer development and progression. Relatively studies have reported that USP15 and USP7 stabilized MDM2 protein levels by removing its ubiquitin chain. In the current study, we studied the cell proliferation status after IU1 treatment and the USP14-MDM2 protein interaction in cervical cancer cells. This study experimentally revealed that IU1 treatment reduced MDM2 protein expression in HeLa cervical cancer cells, along with the activation of autophagy-lysosomal protein degradation and promotion of ubiquitin-proteasome system (UPS) function, thereby blocked G0/G1 to S phase transition, decreased cell growth and triggered cell apoptosis. Thus, these results indicate that IU1 treatment simultaneously targets two major intracellular protein degradation systems, ubiquitin-proteasome and autophagy-lysosome systems, which leads to MDM2 degradation and contributes to the antitumor effect of IU1.

Previous studies have shown that the main function of VASP is to regulate the cytoskeleton and play an important role in promoting tumor cell metastasis. In this study, we first reveal that VASP is located in the nucleus of breast cancer cells and elucidate a Wnt/β-catenin/VASP positive feedback loop. We identify that VASP is a target gene of Wnt/β-catenin signaling pathway, and activation of Wnt/β-catenin signaling pathway can significantly upregulate VASP protein expression, while upregulated VASP protein can in turn promote translocation of β-catenin and DVL3 proteins into the nucleus. In the nucleus, VASP, DVL3, β-catenin, and TCF4 can form VASP/DVL3/β-catenin/TCF4 protein complex, activating Wnt/β-catenin signaling pathway, and promoting the expression of target genes VASP, c-myc, and cyclin D1. Thus, our study reveals that there is a Wnt/β-catenin/VASP malignant positive feedback loop in breast cancer, which promotes the proliferation and migration of breast cancer cells, and breaking this positive feedback loop may provide new strategy for breast cancer treatment.

Data management is an administrative mechanism that involves the acquisitions, validations, storage, protection, and processing of data needed by its users to ensure that data are accessible, reliable, and timely. It is a challenging task to manage protections for information properties. With the emphasis on distributed systems and Internet-accessible systems, the need for efficient information security management is increasingly important. In the paper, artificial intelligence-assisted dynamic modeling (AI-DM) is used for data management in a distributed system. Distributed processing is an effective way to enhance the efficiency of database systems. Therefore, each distributed database structure’s functionality depends significantly on its proper architecture in implementing fragmentation, allocation, and replication processes. The proposed model is a dynamically distributed internet database architecture. This suggested model enables complex decision-making on fragmentation, distribution, and duplication. It provides users with links from anywhere to the distributed database. AI-DM has an improved allocation and replication strategy where no query performance information is accessible at the initial stage of the distributed database design. AI-DM findings show that the proposed database model leads to the reliability and efficiency of the enhanced system. The final results are obtained by analyzing the dynamic modeling ratio is 87.6%, increasing decision support ratio is 88.7%, the logistic regression ratio is 84.5%, the data reliability ratio is 82.2%, and the system ratio is 93.8%.

Big data is an unstructured data set with a considerable volume, coming from various sources such as the internet, business organizations, etc., in various formats. Predicting consumer behavior is a core responsibility for most dealers. Market research can show consumer intentions; it can be a big order for a best-designed research project to penetrate the veil, protecting real customer motivations from closer scrutiny. Customer behavior usually focuses on customer data mining, and each model is structured at one stage to answer one query. Customer behavior prediction is a complex and unpredictable challenge. In this paper, advanced mathematical and big data analytical (BDA) methods to predict customer behavior. Predictive behavior analytics can provide modern marketers with multiple insights to optimize efforts in their strategies. This model goes beyond analyzing historical evidence and making the most knowledgeable assumptions about what will happen in the future using mathematical. Because the method is complex, it is quite straightforward for most customers. As a result, most consumer behavior models, so many variables that produce predictions that are usually quite accurate using big data. This paper attempts to develop a model of association rule mining to predict customers’ behavior, improve accuracy, and derive major consumer data patterns. The finding recommended BDA method improves Big data analytics usability in the organization (98.2%), risk management ratio (96.2%), operational cost (97.1%), customer feedback ratio (98.5%), and demand prediction ratio (95.2%).

There were 376 million migrants in China by 2020, who made significant contributions to urban development. However, they used limited medical services and had lower self-reported health status than inflow city residents. Based on this, this study uses the cross-sectional data of the 2017 China Migrants Dynamic Survey (CMDS) to construct a multiple linear regression model to empirically study the role of health education in improving medical services utilization for migrants. It finds that compared to migrants without health education, the probability of the medical service utilization for migrants with health education has increased significantly, and counseling is more effective than other methods for health education. This promotion effect of health education has been established after a series of robustness tests. Furthermore, this study finds that the closer the migrants are to medical service resources, the greater the effect of health education on medical services utilization for migrants. The heterogeneity test shows that the effect of health education on medical services utilization for migrants is greater among the non-elderly and those with lower education levels. From the perspective of health education, the findings in this study provide empirical evidence to support the government in formulating policies to improve the utilization of medical services for migrants and reduce health inequality.

In China, early childhood care and education services for children under the age of three are neglected to some extent. Based on survey data from the Health Commission in Sichuan Province of China, this study analyzes the situation of early childhood care and education services in Sichuan through a qualitative method, using an analytical framework of matching the demand and supply. The findings reveal a mismatch between demand and supply of early childhood care and education services. This gap is likely to have a negative impact on children's self-development, family stability, and even the construction of national early childhood care and education service system. Drawing on the findings, suggestions for improving the mismatch between demand and supply are provided at the state, community and institution levels.

Background: Rural-to-urban migration has increased rapidly in China since the early 1980s, with the number of migrants reaching 376 million in 2020 (National Bureau of Statistics [NBS], 2020). Despite this sharp trend and the significant contributions that the migrants have made to urban development, migrant workers have had very limited access to the social insurance that the majority of urban workers have enjoyed. Methods: Based on the background of the social insurance system adjustment in Chengdu in 2011, we establish a difference-in-differences (DID) model to empirically test the impacts of change in social insurance policy contribution rates on migrant workers' social insurance participation rates, using the China Migrants Dynamic Survey (CMDS) data from 2009-2016.Results: The social insurance participation rate of migrant workers was significantly reduced after they are incorporated into the urban worker insurance system. Meanwhile, there is no significant change in the wages of migrant workers, but the working hours became longer and the consumption level turned lower. That is to say, simply changing the social insurance model of migrant workers from "comprehensive social insurance" to "urban employee insurance" reduces the incentives for migrant workers to participate in the insurance and harm the overall welfares of migrant workers.Conclusion: The design of the social security policy is an important reason for lower participation rate of migrants. Therefore, it is necessary to solve the problem of insufficient incentives through targeted social security policies. Specifically, the first is to formulate a social security policy contribution rate suitable for the migrants. The second is to establish a comprehensive social security policy and gradually integrate the social security system.

Breast cancer is one of the most common malignant tumors among women worldwide. About 70‐75% of primary breast cancers belong to estrogen receptor (ER)‐positive breast cancer. In the development of ER‐positive breast cancer, abnormal activation of the ERα pathway plays an important role and is also a key point leading to the failure of clinical endocrine therapy. In this study, we found that the small molecule peptide chlorotoxin (CTX) can significantly inhibit the proliferation, migration and invasion of breast cancer cells. In in vitro study, CTX inhibits the expression of ERα in breast cancer cells. Further studies showed that CTX can directly bind to ERα and change the protein secondary structure of its LBD domain, thereby inhibiting the ERα signaling pathway. In addition, we also found that vasodilator stimulated phosphoprotein (VASP) is a target gene of ERα signaling pathway, and CTX can inhibit breast cancer cell proliferation, migration, and invasion through ERα/VASP signaling pathway. In in vivo study, CTX significantly inhibits growth of ER overexpressing breast tumor and, more importantly, based on the mechanism of CTX interacting with ERα, we found that CTX can target ER overexpressing breast tumors in vivo. Our study reveals a new mechanism of CTX anti‐ER‐positive breast cancer, which also provides an important reference for the study of CTX anti‐ER‐related tumors.

Breast cancer is one of the most common malignant tumors worldwide. Metastasis remains the leading cause of death in breast cancer patients. Research on the mechanism of breast cancer metastasis has become a core issue in breast cancer research. Our previous series of studies have shown that VASP, as a key oncogene, plays an important role in the development of various tumors such as breast cancer. In this study, we find that miR-638 can target to inhibit VASP expression, and Lin28 acts as an RNA-binding protein to regulate the processing of miR-638, which inhibits its maturation and promotes the expression of VASP. In addition, we also find that CREB1 acts as a transcription factor that binds to the promoter of Lin28 gene and activates the Lin28/miR-638/VASP pathway. Furthermore, CREB1 can also directly bind to the promoter of VASP, and activate VASP expression, forming a CREB/Lin28/miR-638/VASP interactive network, which plays an important role in promoting cell proliferation and migration in breast cancer. Our study explained the mechanism of CREB1/Lin28/miR-638/VASP network promoting the development of breast cancer, which further elucidated the mechanism of VASP as a key oncogene, and also provided a theoretical basis for expanding new approaches to tumor biotherapy.

Intelligent manufacturing is a new direction for the transformation and upgrading of manufacturing industry. This study constructs regression model and uses the balanced panel data of 30 provincial-level regions from 2008 to 2016 to explores the impact of the construction and promotion of intelligent manufacturing CPS strategic capabilities on the upgrading of manufacturing structure from the perspective of value co-creation theory. The empirical results show that CPS strategic capability has a significant positive impact on the elevation of the manufacturing structure, namely for every 1% increase in CPS strategic capability, the advanced level of manufacturing structure in the sample area increases by an average of 34.8%, and the impact of CPS strategic capability on the elevation is more prominent in economically developed regions and regions with a high level of manufacturing elevation. Mechanism analysis shows that CPS strategic capabilities have optimized and promoted the upgrading of manufacturing structure from five levels: information mapping capability, digital value-added capability, resource coordination capability, intelligent analysis capability and value co-creation capability. On this basis, three suggestions are summarized: increase the input of intelligent innovation, strengthen the optimization of organizational resources, improve the value co-creation ability of manufacturing enterprises, and finally realize the upgrading of manufacturing value chain.

Will aging definitely depress economic growth? Based on the panel data of 31 provinces in China from 2007 to 2017, this paper proposes research hypotheses from the perspective of health investment and technology innovation and then conducts an empirical test of fixed effects panel model based on the Cobb-Douglas production function to prove the relationship between aging and economic growth. Consistent with the mainstream literature, this paper finds that aging does have a significant negative impact on economic growth, that is, for every 1% of population aging, economic growth will decrease 0.089%, but the interaction between aging and health investment or aging and technological innovation on economic growth is significantly positive, namely 0.061%, 0.087% respectively. This means that aging can notably promote economic growth through the paths of health investment and technological innovation. Obviously, The final effect of aging on economic growth depends on the combination of negative effect and positive effect. The findings of this research suggest giving full play to the economic effects of health investment and technological innovation, so as to realize the balanced development of healthy aging, innovation leading, and economic growth.

Backguroud: Breast cancer is one of the most threatening diseases for women, whose metastasis and recurrence are important causes of death in breast cancer patients. Vasodilator-stimulated phosphoprotein (VASP) is a cytoskeletal regulatory protein that promotes invasion and metastasis of tumor cells by regulating cell migration. Bioinformatics data indicated that H3K4me3, WDR5 and MYC co-enriched in the VASP promoter region. Aims: The purpose of this study is to demonstrate the regulatory function and mechanism of WDR5-MYC nexus complex on VASP in breast cancer.Method: In this present study, the expression of VASP in breast cancer and adjacent normal tissues was detected by RT-qPCR. The enrichment of H3K4me3, WDR5 and MYC on the VASP promoter was analyzed by ChIPseeker R package and verified by ChIP-PCR. The interaction of H3K4me3, WDR5 and MYC in breast cancer cells was detected by immunoprecipitation and immunofluorescence. Transcriptional activation function of MYC on VASP was detected by site-directed mutagenesis and dual fluorescence reporter system. The regulatory effect of WDR5 on breast cancer cell migration was tested by wund healing and transwell.Result: VASP is up-regulated in breast cancer tissues as compared with adjacent normal tissues. There is interaction between H3K4me3, WDR5 and MYC and co-enrichment on the VASP promoter. MYC can activate VASP transcription by binding to the VASP promoter-842 binding site. WDR5 and MYC can enhance the migration ability of breast cancer cells by up-regulating VASPConclusion: Our results suggest that WDR5-MYC nexus can activate the transcription of VASP by binding to the VASP promoter region, and promote the migration of breast cancer by up-regulating the expression level of VASP.

Additional file 2: Table S1. The ratio of circ-to-linear of circSMARCA5 (expression of circRNA / linear host genes) and clinical pathologic characteristics of breast cancer.

Additional file 1: Figure S1. The expression level of SMARCA5 and circSMARCA5 in blood and tisssues sample of breast cancer patients health volunteers and tisssues sample of renal cancer. Figure S2. RNA FISH showing circSMARCA5 was mainly expressed in the nucleus. Figure S3. circSMARCA5 decreases the expression of SMARCA5 in MCF-7 cells. Figure S4. The protein level of SMARCA5 in breast cancer and adjacent normal tissues. Figure S5. The expression correlation of circSMARCA5 and SMARCA5in different tumors. Figure S6. circSMARCA5 overexpression downregulated the protein levels of SMARCA5 while upregulating the truncated SMARCA5 (ΔSMARCA5) protein levels. Figure S7. Fragmented genomic DNA for DRIP-qPCR experiments. Figure S8. The secondary structure of circSMARCA5 and circSMARCA5-mut. Figure S9. circSMARCA5 has no significant effect on the proliferation and migration ability of breast cancer cells. Figure S10. The truncated protein ΔSMARCA5 is a nonfunctional protein product. Figure S11. Immunofluorescence assay using a γH2AX antibody showing that the cotransfection of ANT in circSMARCA5-overexpressing cells can abrogate γH2AX levels inducedby circSMARCA5 but the cotransfection of ANT-mut cannot. Figure S12. ANT significantly decreased the degree of colocalization between circSMARCA5 and its cognate DNA locus. Figure S13. (A) MCF-7 cells expressing control vector, circSMARCA5 or circSMARCA5-mut were treated with cisplatin or bleomycin in concentration gradient for 24 h, and CCK8 was used to measure cell viability. Figure S14. circSMARCA5 downregulate SMARCA5 and suppress DNA damage repair in Hela cell.

Background: Breast cancer is the highest incidence of tumor in women, which seriously threaten women's health. The occurrence and progression of breast cancer is linked to inactivation or downregulation of tumor suppressors, and activation or upregulation of oncogenes. However, the mechanism of PAK7 involving in the occurrence and progression of breast cancer is not yet fully understood. Methods: PAK7 expression was analyzed by RT-qPCR and immunohistochemistry and correlated with clinicopatholgical parameters in breast cancer tissue microarray. The effects of PAK7 on breast cancer cells were detected by CCK-8 assay, colon formation assay, wound healing and transwell assays, and flow cytometry. The relationship between PAK7 and Wnt/β-catenin signaling pathway was determined by western blotting, TOP/FOP flash, co-Immunoprecipitation and co-localization assays. Results: PAK7 expression was significantly increased in breast cancer tissues and positively correlated with pathological differentiation and TNM stage of breast cancer. Overexpression of PAK7 could significantly promote proliferation and migration of breast cancer cells, and inhibit apoptosis. In contrast, PAK7 knockdown significantly inhibited the proliferation and migration of breast cancer cells and promoted apoptosis. In addition, PAK7 could activate Wnt/β-catenin signaling pathway in breast cancer cells. Further study found that PAK7 could directly bind to GSK3β and β-catenin, and regulate β-catenin degradation by phosphorylating GSK3β. Conclusions: Our study demonstrated that PAK7, as an oncogene, involved in breast cancer progression by activating the Wnt/β-catenin signaling pathway, suggesting that the potential applicability of PAK7 as a target for breast cancer treatment.

To investigate correlations between excision repair cross-complementation group 1 (ERCC1) and 2 (ERCC2) polymorphisms and osteosarcoma prognosis, we conducted a meta-analysis of studies published through October 2016. Studies were identified in the PubMed, ScienceDirect, Springer, and Web of Science databases using preferred reporting items for systematic reviews and meta-analyses (PRISMA). Odds ratios (ORs) or hazard ratios (HRs) and their 95% confidence intervals (CIs) for overall survival (OS), tumor response (TR), and event-free survival (EFS) were estimated. Our meta-analysis included eleven studies in which four SNPs (ERCC1 rs11615 and rs3212986, ERCC2 rs13181 and rs1799793) reportedly associated with osteosarcoma prognosis were investigated. Each of these studies scored > 6 on the Newcastle-Ottawa Scale (NOS). We found that only one SNP, ERCC1 rs11615, correlated with improved OS and TR. The HR of T vs. C for OS was 1.455 (T/C, 95% CI = 1.151–1.839, P = 0.002, I2 = 37.80%). The OR of T vs. C for good TR was 0.554 (T/C, 95% CI = 0.437–0.702, P < 0.001, I2 = 0%). Few significant outcome was observed in subgroup analyses stratified based on study characteristics with adjustments for potential confounders. Our results suggest that ERCC1 rs11615 CC is associated with a better clinical outcome. This suggests rs11615 may be a useful genetic marker for predicting osteosarcoma prognosis.

Gastric cancer (GC) is one of the most common malignant neoplasms of the digestive system, with China leading in terms of morbidity and mortality rates. Betulinic acid (BA) is a widely-occurring pentacyclic triterpenoid that has been reported to exhibit potent anti-inflammatory, antioxidant, and antitumor activities. BA can combat tumors by inducing apoptosis, regulating cell cycle, and inhibiting autophagy, but its mechanism of action in the context of GC is unclear. A preliminary study found that higher expression of vasodilator-stimulated phosphoprotein (VASP) was correlated with migration in the GC cell line. In this study, BGC-823 cells and MNK45 cells were treated with BA for investigating its effect on the proliferation and migration of cells. Moreover, the expression of VASP and upstream signal molecules were also investigated in this background. The results showed BA could inhibit the proliferation and migration the GC cells. Furthermore, NF-κB acted as a transcription factor to upregulate VASP expression. Moreover, BA could downregulate the expression of VASP at the protein and mRNA level by inhibiting NF-κB activity. In conclusion, these results suggest that BA could inhibit the expression of VASP by negatively regulating NF-κB, thereby inhibiting the proliferation and migration of the GC cells. Our study provides a theoretical basis for exploring the molecular mechanism underlying BA-induced inhibition of proliferation and migration in GC cells.

The important role of LncRNA in the development of breast cancer is attracting more and more attention. In the previous study, we found that the expression level of LncRNA SNHG6 in breast cancer tissues and cells was significantly increased, but its mechanism in the development of breast cancer was still unclear. Our study found that knockdown of SNHG6 significantly inhibited the proliferation, migration and invasion of breast cancer cells MCF-7 and MDA-MB-231 cells. Further study showed that knockdown of SNHG6 significantly inhibited the expression level of VASP. More importantly, SNHG6 and VASP both can bind directly to miR-26a, suggesting that SNHG6 could act as a ceRNA to sponge miR-26a, thereby promoting the expression of VASP, which leading to activated proliferation, migration and invasion of breast cancer cells. Taken together, this study revealed the important role of the SNHG6/miR-26a/VASP regulatory network in the development of breast cancer, and provided a reference for exploring new pathogenesis and biomarkers of breast cancer.

With rapid urbanization and industrialization, the population of metropolis in China is increasing. Previous studies suggest that population agglomeration would have a significant impact on air pollution in cities. Using a panel dataset of 30 provincial capital cities during 2013-2017, as well as days of air quality equal to or above Grade II as air pollution indicators, the results show that an increase of population density will improve air quality in large cities. Through the mediation effect test, this paper found that tertiary industry is the mediation channel of population agglomeration to reduce air pollution. An increase of population density in big cities is conductive to increasing the proportion of tertiary industry, thereby reducing the proportion of seriously polluting secondary industry, and reducing air pollution.