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Background. With the development of sequencing technology, an increasing number of biomarkers have been identified in ovarian cancer (OC). However, there have been few comprehensive analyses of CRIP1 in patients with OC. Methods. Logistic regression analysis was conducted to analyze the correlations between clinical characteristics and CRIP1 expression. Kaplan-Meier survival analysis was used to explore the difference in survival in each clinical subgroup. In addition, univariate and multivariate Cox regression analyses were further used to confirm the independent prognostic values of CRIP1. We further constructed ceRNA network based on the difference analysis. Subsequently, we used the ssGSEA algorithm to excavate the correlation between CRIP1 and tumor-infiltrating immune cells. Moreover, the potential biological functions of CRIP1 were investigated by gene function annotation. Finally, we knocked down CRIP1 gene for preliminary biological function verification in A2780 and SKOV-3 cell lines. Results. The overexpression of CRIP1 was confirmed in The Cancer Genome Atlas (TCGA) cohort, immunohistochemistry, and OC cell lines. CRIP1 overexpression was correlated with the FIGO stage according to a logistic regression analysis that used the median of CRIP1 expression as a categorization of the dependent variable. Survival analysis revealed that CRIP1 was associated with a poor prognosis in most clinical subgroups and acts as an independent prognostic marker in OC patients. In immuno-bioinformatics analysis, CRIP1 is associated to majority of immune cells. This is noteworthy given that we identified that the ceRNA network based on CRIP1 may regulate progression in OC. In addition, gene enrichment analysis suggested CRIP1 may be involved in the JAK-STAT signaling pathway, etc. Finally, we found that knockdown CRIP1 could inhibit the proliferation of OC cells. Conclusion. We provided robust evidences that CRIP1 is an indicator of poor prognosis and a potential target for immunotherapy in patients with OC.

Objective. This research is aimed at investigating the relationship between liver fibrosis in viral hepatitis and macrophage colony-stimulating factor (M-CSF), tissue inhibitor of matrix metalloproteinase (TIMP-1), and ceruloplasmin (CER) in serum level. Methods. Patients were randomly selected among those admitted to our hospital, and 60 healthy volunteers were chosen to serve as control participants. The levels of serum M-CSF, CER, and TIMP-1 were compared. According to the severity of their liver fibrosis, patients with CHB were separated into four groups: S1, S2, S3, and S4. Serum levels of M-CSF, CER, and TIMP-1 were correlated with liver fibrosis and hepatitis markers, and the diagnostic usefulness of the three indices was assessed with liver cirrhosis patients. Results. Increases in M-CSF and TIMP-1 in the CHB group but decreases in CER were statistically significant ( P < 0.05 ). Serum levels of M-CSF, CER, TIMP-1, HA, PC-III, C-IV, and LN differed significantly across the four study groups ( P < 0.05 ). Over time, as liver fibrosis worsened, we observed a progressive uptick in M-CSF, TIMP-1, LN, HA, C-IV, and PC-III levels and a progressive downtick in CER levels, with significant ( P < 0.05 ) differences between the groups. There was a significant positive correlation between liver fibrosis and serum M-CSF, PC-III, TIMP-1, HA, LN, and C-IV levels in the CHB group ( P < 0.05 ) and a significant negative correlation between serum CER and these same factors ( P < 0.05 ). The AUC of 0.956 for diagnosing the S4 stage was greater than that of 0.857, 0.851, and 0.817 for M-CSF, CER, and TIMP-1, respectively. Conclusions. In CHB patients, the liver fibrosis degree is associated with the M-CSF, CER, and TIMP-1 levels, and the combined clinical detection of these three markers has better diagnostic significance.

This study aimed to explore the expression profile, prognostic value, regulatory effect, and the underlying mechanism of dysregulation of phosphoglycerate kinase 1 (PGK1) in high-risk human papillomavirus (HPV)-positive cervical epithelial squamous cell carcinoma (CESC). Bioinformatic analysis was performed using the CESC subset of The Cancer Genome Atlas (TCGA)-Cervical Cancer (CESC) and normal cervix in The Genotype-Tissue Expression (GTEx) project. HPV-16 positive CaSki and SiHa cells were used as in vitro cell models. Results showed that compared to the normal cervix, CESC tissues had significantly higher expression of PGK1. CESC patients with the higher 50% expression of PGK1 had substantially shorter disease-specific survival (DSS), and progression-free survival (PFS) compared to the cases with the lower 50% expression of PGK1. PGK1 knockdown impaired, but PGK1 overexpression enhanced the proliferation, colony formation, aerobic glycolytic activities (lactate production, intracellular ATP levels, glucose uptake, and extracellular acidification rate), migration, and invasion of CaSki and SiHa cells. HPV-16 E6/E7 knockdown in CaSki and SiHa cells had limited influence on PGK1 transcription but significantly decreased the half-life of PGK1 protein. E6/E7 knockdown mediated PGK1 downregulation could be blocked by adding MG-132. PGK1 poly-ubiquitination was significantly enhanced after E6/E7 knockdown. In conclusion, this study showed that PGK1 expression might serve as a prognostic biomarker in cervical cancer. Its upregulation contributes to enhanced aerobic glycolysis, migration, and invasion of CESC cells. HPV16 E6/E7 stabilizes PGK1 protein by reducing its poly-ubiquitination.

Long noncoding RNA lung cancer associated transcript 1 (LUCAT1) has been shown to be a lncRNA that facilitates the development and progression of several tumours. However, the evidence of LUCAT1 modulating the growth and metastasis of cervical cancer (CC) were still lacking. The present study aimed to explore the expression pattern, biological function and potential mechanism of LUCAT1 in CC. In this study, we, first, confirmed that LUCAT1 acted as an up-regulated lncRNA by analyzing the data from GCTA dataset and RT-PCR in both CC tissues and cell lines. We also showed that TINCR overexpression is induced by nuclear transcription factor SP1. Then, clinical assays showed that LUCAT1 was associated with advanced clinical progression and poor prognosis of CC patients. Importantly, multivariate Cox model confirmed that LUCAT1 expression was an independent prognostic factor for both 5-year overall survival in CC. Then, lost-function assays revealed that knockdown of LUCAT1 significantly suppressed CC cells proliferation, colony formation, migration, invasion and EMT by a series of cells experiments. Mechanistically, Bioinformatic tools predicted that miR-181a may target LUCAT1, which was confirmed using luciferase reporter assay and RNA immunoprecipitation (RIP) assays. Overall, our findings showed that SP1-activated LUCAT1 exerts an oncogenic function in CC by binding to miR-181a, suggesting that miR-181a may be a ponderable and promising therapeutic target for CC.

BACKGROUND Ovarian cancer is one of the most common gynecological malignancies and mortality ranks the highest in cancer-associated death in females' worldwide. Here, we attempted to evaluate the effect of DANCR on the biological behavior of transforming growth factor-s (TGF-s) stimulated ovarian cancer cells. MATERIAL AND METHODS The expression of DANCR in ovarian cancer cells (A2780 and SKOV3) treated with TGF-s were detected by quantitative real-time polymerase chain reaction (qRT-PCR). DANCR silencing was constructed using lentiviral transfection in ovarian cancer cells. The Cell Counting Kit-8 (CCK-8), flow cytometry and Transwell assays were performed to measure some cytology index. Western blot was utilized to explore the effect of DANCR on Kruppel-like factor 5 (KLF5) expression. RESULTS The expression of DANCR in cancer cells (A2780 and SKOV3) treated with TGF-s was significantly higher. DANCR silencing suppressed cell viability, migration and invasion, and induced cell apoptosis of TGF-s treated ovarian cancer cells. Bioinformatics analysis showed that DANCR served as a sponge for miR-214, and also showed that KLF5 was targeted by miR-214. In addition, DANCR could inhibit the expression of KLF5. CONCLUSIONS We are the first to report that knockdown of DANCR could affect the biological process of ovarian cancer cells treated with TGF-s by sponging miR-214, which may provide new therapeutic ideas of ovarian cancer.

The WRKY transcription factors, a large family of proteins in plants, are involved in multiple developmental and biological processes including response to phytohormones and abiotic stress. However, little information is available regarding the WRKY family in Eucalyptus, which has been the most widely planted hardwood trees in tropical and subtropical areas. In this study, a total of 79 WRKY genes (named as EgrWRKY1-79) were identified from the Eucalyptus grandis genome and classified into three main groups according to the phylogenetic analysis, which was further supported by their gene structure and conserved motifs. Of which, 28 EgrWRKYs were involved in tandem duplication but none for segmental duplication, indicating that tandem duplication was the main cause for the expansion of WRKY gene family in E. grandis. Subsequently, expression profiles of EgrWRKY genes in eight different tissues and in response to treatments of three hormones (SA, JA, and BR) and two abiotic stresses (salt and cold) were analyzed. The results revealed that the EgrWRKY genes had differential expression in their transcript abundance and they were differentially expressed in response to plant hormones and salt and cold stresses, suggesting their contributions to plant developmental processes as well as abiotic stresses with the involvement of hormone signaling transduction. Taken together, these findings will increase our understanding of EgrWRKY gene family involved in abiotic stresses and hormone signaling transduction, and also will provide some stress-responsive candidate EgrWRKY genes for further characterization of their functions in Eucalyptus.

In this study, we aimed to assess the independent prognostic value of miR-361-3p in terms of overall survival (OS) and recurrence-free survival (RFS) in cervical cancer, as well as its possible regulative network. A retrospective analysis was performed by using data from the Cancer Genome Atlas-Cervical Cancer (TCGA-CESC). Results showed that decreased miR-361-3p expression was associated with lymphovascular invasion and poor responses to primary therapy. The patients with recurrence and the deceased cases had substantially lower miR-361-3p expression compared to their respective controls. By generating Kaplan-Meier curves of OS and RFS, we found that high miR-361-3p expression was associated with better survival outcome. More importantly, univariate and multivariate analysis confirmed that high miR-361-3p expression was an independent indicator of favorable OS (HR: 0.377, 95% CI: 0.233–0.608, p<0.001) and RFS (HR: 0.398, 95% CI: 0.192–0.825, p=0.013). By performing bioinformatic analysis, we identified 24 genes that were negatively correlated with miR-361-3p expression. Among the potential targeting genes, SOST, MTA1, TFRC, and YAP1 are involved in some important signaling pathways modulating cervical cancer cell invasion, migration, and drug sensitivity. Therefore, it is meaningful to verify the potential regulative effect of miR-361-3p on the expression of these genes in the future.

Circular RNAs (circRNAs) have been shown to be involved in the development of cancer. The aim of the present study was to investigate the role of circRNA SMARCA5 (cSMARCA5) in human cervical cancer. In the present study, cSMARCA5 expression was upregulated in cervical cancer tissues and cell lines. Furthermore, the proliferation rate of cells transduced with viral plasmids expressing small interfering RNA targeting cSMARCA5 was downregulated. Bioinformatics analysis predicted that microRNA (miR)‑432 targeted cSMARCA5, and miR‑432 was able to interact with epidermal growth factor receptor (EGFR) by binding to its 3'‑untranslated region. The expression levels of EGFR, ERK1 and ERK2 were increased in cervical cancer tissues. Furthermore, correlation analysis revealed that cSMARCA5 levels were positively correlated with ERK1 and ERK2 levels. In conclusion, the present findings suggested that cSMARCA5 may play an important role in the progression of cervical cancer via the ERK signaling pathway by modulating miR‑432.

Low Impact Development Best Management Practices (LID-BMPs) have in recent years received much recognition as cost-effective measures for mitigating urban runoff impacts. In the present paper, a procedure for LID-BMPs planning and analysis using a comprehensive decision support tool was proposed. A case study was conducted to the planning of an LID-BMPs implementation effort at a college campus in Foshan, Guangdong Province, China. By examining information obtained, potential LID-BMPs were first selected. SUSTAIN was then used to analyze four runoff control scenarios, namely: pre-development scenario; basic scenario (existing campus development plan without BMP control); Scenario 1 (least-cost BMPs implementation); and, Scenario 2 (maximized BMPs performance). A sensitivity analysis was also performed to assess the impact of the hydrologic and water quality parameters. The optimal solution for each of the two LID-BMPs scenarios was obtained by using the non-dominated sorting genetic algorithm-II (NSGA-II). Finally, the cost-effectiveness of the LID-BMPs implementation scenarios was examined by determining the incremental cost for a unit improvement of control.

In the present study, the function of microRNA (miR)‑195 on abdominal aortic aneurysm (AAA) and its possible mechanism were investigated. Reverse transcription‑quantitative polymerase chain reaction analysis was used to detect the expression of miR‑195 in patients with AAA. The expression levels of miR‑195 in patients with AAA were effectively increased. The present study also used miR‑195 mimics to increase the expression of miR‑195, and ELISA kits and western blot analysis were used to analyze the levels of interleukin (IL)‑1β and IL‑6, and the protein expression levels of matrix metalloproteinase (MMP)‑2, MMP‑9, tumor necrosis factor (TNF)‑α, nuclear factor (NF)‑κB, vascular endothelial growth factor (VEGF), phosphoinositide 3‑kinase (PI3K) and phosphorylated (p‑)Akt. The overexpression of miR‑195 promoted the levels of IL‑1β and IL‑6, induced the protein expression of MMP‑2 and MMP‑9, upregulated the protein expression of TNF‑α and NF‑κB, and suppressed the protein expression levels of VEGF, PI3K and p‑Akt in angiotensin II‑vascular smooth muscle cells. In addition, TNF‑α promoted the pre‑inflammatory effect of miR‑195 on the protein expression levels of TNF‑α and NF‑κB, levels of IL‑1β and IL‑6, and protein expression levels of MMP‑2 and MMP‑9 in the angiotensin II‑vascular smooth muscle cells. Suppression of PI3K promoted the pre‑inflammatory effect of miR‑195 on the protein expression of PI3K, p‑Akt and VEGF, the levels of IL‑1β and IL‑6, and the protein expression of MMP‑2 and MMP‑9 in angiotensin II‑vascular smooth muscle cells. Combined, these results suggested that miR‑195 suppressed AAA inflammation through the TNF‑α/NF‑κB and VEGF/PI3K/Akt pathways.

China is at present experiencing a very rapid urbanization process, which has brought a number of adverse impacts upon the water environment. In particular, urban runoff quantity and quality control have emerged as one of the key concerns for municipal officials. One of the strategies being considered is the use of a Low Impact Development type of Best Management Practices (LID BMPs) for urban storm water runoff quantity and quality control. In this paper, the situation surrounding urban runoff control in China is reviewed first. Then the conventional strategy and technologies for the construction and management of urban drainage systems are discussed, while exploring their inherent dilemmas. The LID BMPs are then introduced to control urban runoff in the context of urban sustainable water systems. After the comprehensive analysis of the various LID BMPs, the advances in LID BMPs research and practice for urban runoff control in China are investigated and summarized. At last, the difficulties of implementing LID BMPs in China are discussed, and a direction for the future is proposed.

Low impact development best management practices (LID-BMPs) are considered to be cost-effective measures for mitigating the water quantity and quality impact of urban runoff. Currently, there are many types of LID-BMPs, and each type has its own intrinsic technical and/or economical characteristics and limitations for implementation. The selection of the most appropriate BMP type(s) for a specific installation site is therefore a very important planning step. In the present study, a multi-criteria selection index system (MCIS) for LID-BMP planning was developed. The selection indexes include 12 first-level indices and 26 second-level indices which reflect the specific installation site characteristics pertaining to site suitability, runoff control performance, and economics of implementation. A mechanism for ranking the BMPs was devised. First, each individual second-level index was assigned a numeric value that was based on site characteristics and information on LID-BMPs. The quantified indices were normalized and then integrated to obtain the score for each of the first-level index. The final evaluation scores of each LID-BMP were then calculated based on the scores for the first-level indices. Finally, the appropriate BMP types for a specific installation site were determined according to the rank of the final evaluation scores. In order to facilitate the application of the MCIS BMP ranking system, the computational process has been coded into a software program, BMPSELEC. A case study demonstrating the MCIS methodology, using an LID-BMP implementation planning at a college campus in Foshan, Guangdong Province, is presented.

Epigenetic modulation is an important mechanism of miRNA dysregulation in cervical cancer. In this study, we firstly studied how this mechanism contributes to miR-375 downregulation in cervical cancer cells. Then, we further studied the association between miR-375 and MALAT1 (metastasis associated lung adenocarcinoma transcript 1) in epithelial mesenchymal transition (EMT) of the cancer cells. HPV-16 positive SiHa and CaSki cells were used as in vitro model. Our data showed that HPV-16 E6 positively modulated DNMT1 expression in both SiHa and CaSki cells. Knockdown of DNMT1 partly restored miR-375 levels in the cells. The following methylation-specific PCR (MSP) assay and qRT-PCR analysis showed that methylation was common in the promoter region of miR-375 in both SiHa and CaSki cells and demethylation partly restored miR-375 levels in the cells. Therefore, we infer that miR-375 is downregulated partly due to promoter hypermethylation mediated by DNMT1 in HPV-16 positive cervical cancer cells. Our bioinformatics analysis showed that MALAT1 has three putative binding sites with miR-375 and the following dual luciferase assay confirmed two of them. QRT-PCR analysis showed that miR-375 overexpression significantly reduced MALAT1 expression, while MALAT1 overexpression reversely suppressed miR-375 levels. Therefore, we infer that there is a reciprocal regulation between miR-375 and MALAT1 in the cells. In SiHa cells, miR-375 overexpression or MALAT1 siRNA partly restored E-cadherin expression, significantly reduced N-cadherin and also reduced invasion capacity of SiHa cells. Therefore, these results suggest that miR-375 and MALAT1 form a functional axis modulating EMT in cervical cancer.

MiR-21 is an important microRNA (miRNA) modulating radiosensitivity of cervical cancer cells. However, the underlying mechanism of miR-21 upregulation in radioresistant cervical cancer has not been fully understood. In addition, autophagy may either promote or alleviate radioresistance, depending on the types of cancer and tumor microenvironment. How autophagy affects radiosensitivity in cervical cancer and how miR-21 is involved in this process has not been reported. This study showed that miR-21 upregulation in radioresistant cervical cancer is related to HIF-1α overexpression. MiR-21 overexpression decreases PTEN, increases p-Akt, and subsequently increases HIF-1α expression, while miR-21 inhibition results in increased PTEN, decreased p-Akt, and then decreased HIF-1α. Therefore, we inferred that there is a HIF-1α-miR-21 positive feedback loop through the PTEN/Akt/HIF-1α pathway in cervical cancer cells. In addition, we also demonstrated that miR-21 confers decreased autophagy in cervical cancer cells after IR via the Akt-mTOR signaling pathway. Decreased autophagy is one of the potential mechanisms of increased radioresistance in cervical cancer cells. These findings expand our understanding of radioresistance development in cervical cancer.

To determine the survival rates of liver cancer in Qidong during the years 1972-2011, according to the data from a population-based cancer registry, in order to assess the long-term trends for prognosis of this cancer type.The deadline of the last follow-up for survival status of the 28, 398 registered cases was April of 2012. Cumulative observed survival (OS) and relative survival (RS) rates were calculated using Hakulinen's method performed by the SURV3.01 software developed by the Finnish Cancer Registry.The 1-, 3-, 5-, 10-and 15-year OS rates were 15.18%, 6.23%, 4.26%, 2.79% and 2.39%, respectively; the 1-, 3-, 5-, 10-and 15-year RS rates were 15.47%, 6.60%, 4.69%, 3.41% and 3.29%, respectively. For males, these OS rates were 14.95%, 6.05%, 4.06%, 2.67% and 2.26%, and these RS rates were 15.23%, 6.41%, 4.47%, 3.26% and 3.12%, respectively. For females, these OS rates were 15.89%, 6.79%, 4.87%, 3.17% and 2.80%, and these RS rates were 16.20%, 7.20%, 5.37%, 3.87% and 3.82%, respectively. No statistical differences were found between the male and female groups (P0.05). The 5-year RS rates for age groups 15-34, 35-44, 45-54, 55-64, 65-74 and 75+ years-old were 4.42%, 4.29%, 4.96%, 4.67%, 4.67% and 6.35%, and the 10-year RS rates were 3.17%, 2.98%, 3.44%, 3.47%, 3.75% and 11.27%, respectively. Remarkable improvement was seen for the 1-, 3-, 5-, 10-and 15-year OS rates in this setting since the 1980s.The survival outcome from Qidong registered cases with liver cancer has shown gradual progress over the past four decades. Early detection and improvement of therapies may be responsible for the improved prognosis of liver cancer. While the disparity gap of survival between this area and developed countries is narrowing, there is still a need for improving the survival in Qidong.