Retraction notice to "Co infection of respiratory syncytial viruses (RSV) and Streptococcus pneumonia modulates pathogenesis and dependent of serotype and phase variant" [Microb. Pathog. 144 (2020) 104126].

This article has been retracted: please see Elsevier Policy on Article Withdrawal (https://www.elsevier.com/about/our-business/policies/article-withdrawal). This article has been retracted at the request of the Editor-in-Chief. After a thorough investigation, the Editor has concluded that the acceptance of this article was based upon the positive advice of two illegitimate reviewer reports. The reports were submitted from email accounts which were provided to the journal as suggested reviewers during the submission of the article. Although purportedly real reviewer accounts, the Editor has concluded that these were not of appropriate, independent reviewers. This manipulation of the peer-review process represents a clear violation of the fundamentals of peer review, our publishing policies, and publishing ethics standards. Apologies are offered to the reviewers whose identity was assumed and to the readers of the journal that this deception was not detected during the submission process.

Patterned vascularization in a directional ice-templated scaffold of decellularized matrix.

Vascularization is fundamental for large-scale tissue engineering. Most of the current vascularization strategies including microfluidics and three-dimensional (3D) printing aim to precisely fabricate microchannels for individual microvessels. However, few studies have examined the remodeling capacity of the microvessels in the engineered constructs, which is important for transplantation in vivo. Here we present a method for patterning microvessels in a directional ice-templated scaffold of decellularized porcine kidney extracellular matrix. The aligned microchannels made by directional ice templating allowed for fast and efficient cell seeding. The pure decellularized matrix without any fixatives or cross-linkers maximized the potential of tissue remodeling. Dramatical microvascular remodeling happened in the scaffold in 2 weeks, from small primary microvessel segments to long patterned microvessels. The majority of the microvessels were aligned in parallel and interconnected with each other to form a network. This method is compatible with other engineering techniques, such as microfluidics and 3D printing, and multiple cell types can be co-cultured to make complex vascularized tissue and organ models.

Pseudogene DUXAP8 Promotes Cell Proliferation and Migration of Hepatocellular Carcinoma by Sponging MiR-490-5p to Induce BUB1 Expression.

Hepatocellular Carcinoma (HCC) currently remains one of the most lethal malignancies worldwide. Recently, long non-coding RNAs (lncRNAs) had been demonstrated to play a crucial role in the progression of multiple human cancers, including HCC. In this study, we found that lncRNA DUXAP8 was upregulated in tumor samples and served as an oncogene in HCC. Bioinformatics analysis showed that DUXAP8 was significantly associated with the regulation of centrosome organization, homologous recombination, meiotic cell cycle process, sister chromatid segregation, nuclear chromosome segregation, and RNA export from the nucleus. The knockdown of DUXAP8 significantly suppresses cell proliferation and the cell cycle but induces cell apoptosis in HCC. Mechanically, the present study showed that DUXAP8 serves as a sponge of MiR-490-5p to promote the expression of BUB1 in HCC. Although the underlying regulatory mechanisms of DUXAP8 in HCC require further investigation, this study, for the first time, showed that DUXAP8 can serve as a new therapeutic target for HCC.

Co infection of respiratory syncytial viruses (RSV) and streptococcus pneumonia modulates pathogenesis and dependent of serotype and phase variant.

Streptococcus pneumoniae (pneumococcus) is touted to be the generally found pathogen in patients with respiratory issues and there is an epidemiologic linkage present between Respiratory syncytial virus (RSV). This study aim at investigating the interaction between RSV and two serotypes of S. pneumoniae using a distinct animal model and a well-established colonizing pneumococcal strain. Phase variants phenotype of each strain was determined under oblique light. Co infection model was developed using BALB/c mice housed in a BSL-2 facility. Coinfection experiments were performed and number of bacterial colonies was quantified and phase determination was evaluated. RSV was detected in sample through real-time quantitative PCR. Adherence assays were performed to determine adherence of Spn strains and its knock out ΔNanA to nasopharyngeal carcinoma (NPC) epithelial CNE3 cell line. The biofilm viability was determined and phase composition was counted using plate count. Neuraminidase activity was measured in fluorometircassessed using 2'-(4-methylumbelliferyl)-α-D-N-acetylneuraminic acid (MUAN) as substrate as described in earlier literature. The GraphPad Software version 5.01 i.e., GraphPad Prism was used to conduct the statistical analysis. The extent of bacterial colonization was increased significantly (p < 0.05), when the mice were co infected. Nasal epithelium remained intact in mock sample with features of a thick mucociliary border. A small percentage of pneumococci exhibit phase variation between opaque phase and transparent phase. The percentage adherent of both phase were not found to be varying significantly within serotype but it was seen that nonpathogenic type 27 was more adherent. Biofilm formation was selectively more for transparent phase from a mixed-phase inoculum. Adherence of both phase variant of S. pneumoniae to nasopharyngeal epithelial cells 2 h post infection expressed as the percentage of adherent bacteria relative to the inoculum. In absence of viral infection, the nasal colonization of the opaque and the transparent variant was increased many folds, which was a significant differences. The extent of nasal colonization by the ΔNanA mutant strain were significantly reduced post-bacterial infection for both type of wild-type (P < 0.05). The findings explore insights into the interactions occurring between S. pneumoniae and RSV during respiratory infections and pneumococcal acquisition, indicate that pneumococcal serotypes have different ability to cause infection as well as co infections and potentially follow an unappreciated mechanism. Much more research work is needed to further understand the minutiae of this interaction within co-infection process.

The Value of lncRNA GHET1 as a Prognostic Factor for Survival of Chinese Cancer Outcome: A Meta-Analysis.

AIM: There is increasing evidence that high expression levels of the gastric carcinoma highly expressed transcript 1 (GHET1), a long noncoding RNA (lncRNA), are associated with cancer prognosis and may be used as a valuable biomarker for cancer patients. The purpose of this meta-analysis was to analyze existing data to reveal potential clinical applications of GHET1 for cancer prognosis and tumor progression. All of these studies included in this meta-analysis were collected through a variety of retrieval strategies; and the enrolled articles were qualified via the meta-analysis of enrolled studies in epidemiology (MOOSE) and the preferred reporting items for systematic reviews and meta-analyses (PRISMA) checklists. MATERIALS AND METHODS: The literature collection was performed by a comprehensive search through electronic databases for studies published on or before March 10, 2019. These included the Cochrane library, PubMed, Embase, Web of Science, Springer, Science Direct, and three Chinese databases: CNKI, Weipu, and Wanfang. Seven studies that met the specified criteria were analyzed in the present research. RESULTS: The combined results indicate that an elevated GHET1 expression level is significantly associated with poor overall survival (OS) (HR = 2.40, 95% CI: 1.87-3.08, p < 0.001) and tumor progression (III/IV vs. I/II: HR = 1.80, 95% CI: 1.48-2.18, p < 0.001) in multiple cancers. The elevated GHET1 expression was also associated with lymph node metastasis (LNM) (HR = 2.44, 95% CI: 1.86-3.20, p < 0.001) in Chinese cancer patients. Conclusions. The present findings indicate that an increased GHET1 expression level is associated with poor OS, tumor progression, and LNM in patients with multiple tumors and may serve as a useful prognostic biomarker in Chinese cancer patients.

LncRNA PANDAR is a Novel Prognostic Biomarker in Patients with Cancer: a Meta-Analysis.

BACKGROUND: Mounting evidence from recent studies has revealed the association of lncRNA PANDAR expression levels with outcomes in several types of cancer. However, inconsistent results have also been reported, which rationalized a meta-analysis of available data to analyze the prognostic value of lncRNA PANDAR. METHODS: From inception to May 26, 2018, electronic literature databases including PubMed (medline), the Cochrane Library, ScienceDirect, Springer, ISI Web of Knowledge, Wiley Online library, BioMed Central, and Embase were searched for literature collections. The hazard ratios (HR) with 95% confidence interval (95% CI) were utilized to calculate pooled effect size. RESULTS: A total of 1,132 cancer patients were enrolled in the present meta-analysis to assess the prognostic value of PANDAR in various carcinomas. Promoted PANDAR expression was demonstrated to significantly predict unfavorable OS (HR = 1.77, 95% CI: 1.12 - 2.80, p = 0.014) by the random effects model. According to the stratified analyses and meta-regression results, the heterogeneity of present analysis may be attributed to the differences of cancer resources. Furthermore, over-expression of PANDAR was revealed to be effectively predictive of cancer progression (HR = 1.70, 95% CI: 1.41 - 2.05, p < 0.00001) and LNM (HR = 1.71, 95% CI: 1.39 - 2.10, p < 0.00001). CONCLUSIONS: The present findings indicate that increased PANDAR is associated with poor OS in patients with general carcinomas and may serve as a useful clinical prognostic biomarker.

The Value of lncRNA NEAT1 as a Prognostic Factor for Survival of Cancer Outcome: A Meta-Analysis.

The present meta-analysis aimed to analyze available data to identify the prognostic role of NEAT1 in multiple carcinomas. A systematic search was performed by using several computerized databases from inception to June 7, 2017. The quantity of the publications was assessed according to MOOSE checklist. Pooled HRs with 95% CI was calculated to summarize the effect. A total of 12 studies with 3,262 cancer patients were pooled in the analysis to evaluate the prognostic value of NEAT1 in multiple tumors. High expression levels of NEAT1 were demonstrated to be associated with poor OS (HR = 1.71, 95%CI: 1.37-2.14, P < 0.001) and tumor progression (III/IV vs. I/II: HR 1.76, 95%CI: 1.40-2.21, P < 0.00001). Subgroup analysis showed that NEAT1 detection method (qRT-PCR) and sample size (more or less than 100) did not alter the predictive value of NEAT1 on OS in various cancers. According to the meta-regression results, the large heterogeneity of meta-analysis may be attributed to the differences of NEAT1 detection method. Furthermore, elevated NEAT1 expression significantly predicted lymph node metastasis (HR: 2.10, 95%CI: 1.32-3.33, P = 0.002) and distant metastasis (HR: 2.80, 95%CI: 1.60-4.91, P = 0.0003) respectively. The results indicate that NEAT1 expression level is a prognostic biomarker for OS and metastasis in general tumors.

Prognostic value of lncRNA SOX2OT for Chinese cancer patients: A meta-analysis.

SOX2OT has been demonstrated to be aberrantly expressed in several types of cancer and maybe serve as a prognostic marker for cancer patients. However, most individual studies have been limited by small sample sizes and controversial results. Therefore, the present meta-analysis was conducted to analyze available data to reveal the potential clinical application of SOX2OT on cancer prognosis, tumor progression, distance metastasis and lymph node metastasis. Up to February 20, 2017, literature collections were conducted by comprehensive searching electronic databases, including Cochrane Library, PubMed, Embase, BioMed Central, Springer, ScienceDirect, ISI Web of Knowledge, together with three Chinese databases: China National Knowledge Internet (CNKI), Weipu and Wanfang. The hazard ratios (HR) with 95% confidence interval (95% CI) were calculated to assess the strength of the association. Five studies with a total of 481 cancer patients were included in the present meta-analysis. The results indicated that elevated SOX2OT significantly predicted unfavorable overall survival (OS) (HR = 2.44, 95% CI: 1.75-3.39, P<0.0001) and tumor progression (III/IV vs. I/II: HR 1.62, 95%CI: 1.30-2.02, P<0.0001), but failed to predict distant metastasis (HR: 3.30, 95%CI: 0.74-14.61, P = 0.12) and lymph node metastasis (HR: 1.29, 95% CI: 0.87-1.91, P = 0.21). The results revealed that SOX2OT expression level was an independent prognostic biomarker for OS and tumor progression in Chinese cancer patients.

The Value of lncRNA HULC as a Prognostic Factor for Survival of Cancer Outcome: A Meta-Analysis.

AIMS: Growing evidence from recent studies has shown that lncRNA HULC plays a role in the development of multiple carcinomas. This meta-analysis aimed to analyze available data to identify the prognostic value of HULC in multiple tumors. METHODS: A systematic search was performed by using PubMed (medline), Embase, ISI Web of Knowledge, Springer, the Cochrane Library, Scopus, BioMed Central, ScienceDirect, Wanfang, Weipu, and China National Knowledge Internet (CNKI) computerized databases from inception to Nov 30, 2016. The quality of the publications was assessed according to the critical review checklist of the Dutch Cochrane Centre proposed by MOOSE and PRISMA. Pooled hazard ratios (HR) with 95% confidence interval (95% CI) were calculated to summarize the effect. RESULTS: A total of ten studies with 1077 cancer patients were pooled in the present meta-analysis to evaluate the prognostic value of HULC in multiple tumors. High expression levels of HULC were demonstrated to be associated with poor overall survival (OS) (HR=2.44, 95%CI: 1.96-3.03, P=0.000). Subgroup analysis showed that cancer type (digestive or non-digestive disease), residence region (China), sample size (more or less than 100) and follow-up months (more or less than 60) did not alter the predictive value of HULC on OS in various cancers. Additionally, increased HULC expression was found to be moderately associated with tumor stage and progression (III/IV vs. I/II: HR=1.59, 95% CI: 1.31-1.92, P<0.00001). Furthermore, elevated HULC expression significantly predicted distant metastasis (HR=3.90, 95% CI: 1.89-8.02, P=0.0002) and lymph node metastasis (HR=2.04, 95% CI: 1.03-4.05, P=0.04) respectively. No significant heterogeneity was observed among studies except lymph node metastasis. CONCLUSION: The results indicate that HULC expression level is an independent prognostic biomarker for unfavorable OS and metastasis in general tumors.

Prognostic Value of microRNA-9 in Various Cancers: a Meta-analysis.

Recently, there are more and more evidences from studies have revealed the association between microRNA-9 (miR-9) expression and outcome in multiple cancers, but inconsistent results have also been reported. It is necessary to rationalize a meta analysis of all available data to clarify the prognostic role of miR-9. Eligible studies were selected through multiple search strategies and the quality was assessed by MOOSE. Data was extracted from studies according to the key statistics index. All analyses were performed using STATA software. Twenty studies were selected in the meta-analysis to evaluate the prognostic role of miR-9 in multiple tumors. MiR-9 expression level was an independent prognostic biomarker for OS in tumor patients using multivariate and univariate analyses. High expression levels of miR-9 was demonstrated to associated with poor overall survival (OS) (HR = 2.23, 95 % CI: 1.56-3.17, P < 0.05) and recurrence free survival/progress free survival (RFS/PFS) (HR = 2.08, 95 % CI: 1.33-3.27, P < 0.05). Subgroup analysis showed that residence region (China and Japan), sample size, cancer type (solid or leukemia), follow-up months and analysis method (qPCR) did not alter the predictive value of miR-9 on OS in various cancers. Furthermore, no significant associations were detected for miR-9 expression and lymph node metastasis or distant metastasis. The present results suggest that promoted miR-9 expression is associated with poor OS in patients with general cancers.

Downregulation of KDR expression induces apoptosis in breast cancer cells.

Angiogenesis plays a crucial role in the growth, invasion and metastasis of breast cancer. Vascular endothelial growth factors (VEGFs) and their receptors (VEGFRs) are the key regulators of tumor angiogenesis. VEGFR-2, known as the kinase insert domain receptor (KDR), is a key receptor involved in malignant angiogenesis. We previously showed that knocking down KDR with short interference RNA (KDR-siRNA) markedly decreased KDR expression and suppressed tumor growth in a xenograft model. However, the mechanisms underlying the anti-cancer effects of KDR-siRNA are not clearly understood. This study aimed to elucidate the molecular mechanisms that induce apoptosis in human breast cancer MCF-7 cells after transfection with KDR-siRNA. We studied the effects of KDR-siRNA on proliferation, apoptosis, antiapoptotic and pro-apoptotic proteins, mitochondrial membrane permeability, cytochrome c release and caspase-3 activity. The results indicated that KDR-siRNA treatment significantly inhibited the proliferation and induced the apoptosis of MCF-7 cells, reduced the levels of the anti-apoptotic proteins, Bcl-2 and Bcl-xl, and increased the level of the pro-apoptotic protein Bax, resulting in a decreased Bcl-2/Bax ratio. KDR-siRNA also enhanced the mitochondrial membrane permeability, induced cytochrome c release from the mitochondria, upregulated apoptotic protease-activating factor-1 (Apaf-1), cleaved caspase-3, and increased caspase-3 activity in MCF-7 cells. Furthermore, KDR-siRNA-induced apoptosis in MCF-7 cells was blocked by the caspase inhibitor Z-VAD-FMK, suggesting a role of caspase activation in the induction of apoptosis. These results indicate that the Bcl-2 family proteins and caspase-related mitochondrial pathways are primarily involved in KDR-siRNAinduced apoptosis in MCF-7 cells and that KDR might be a potential therapeutic target for human breast cancer treatments.

The knockdown of c-myc expression by RNAi inhibits cell proliferation in human colon cancer HT-29 cells in vitro and in vivo.

We investigated the effects of RNA interference-mediated silencing of the c-myc gene on celluar proliferation and apoptosis in human colon cancer HT-29 cells in vitro and in vivo. A small interfering RNA (siRNA) targeting c-myc was designed, the DNA template was synthesized, and the siRNA was obtained by in vitro transcription. After siRNA transfection into HT-29 and human neuroblastoma IMR-32 cells with Lipofectamine 2000, the proliferation of the HT-29 and IMR-32 cells was assessed via 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium bromide (MTT) colorimetry, and Hoechst 33258 staining was used to observe cell apoptosis. Following gene transfer to HT-29 cells, the expression of c-myc mRNA was examined via reverse transcription polymerase chain reaction, and the level of the protein via Western blot assay. Growth curves were constructed and in vivo experiments were performed on nude mice to assess the effects of c-myc silencing on tumor growth. The c-myc expression in the tumor tissue was measured by reverse transcription polymerase chain reaction and subsequently by immunohistochemistry. Our paper demonstrates that the delivery of siRNA directed against c-myc not only efficiently down-regulated the expression of c-myc, inhibited the proliferation of HT-29 cells and induced apoptosis in vitro, but also suppressed the growth of colon cancer cells in vivo.

The mechanisms on apoptosis by inhibiting VEGF expression in human breast cancer cells.

This study investigated apoptotic mechanisms of down-expression vascular endothelial growth factor (VEGF) by short interfering RNA (siRNA) in human breast cancer MCF-7 cells. Human breast cancer cells were evaluated for the expression of VEGF and VEGF receptor 2 (VEGFR-2). siRNA targeting VEGF mRNA were chemically synthesized and transfected into cells with Lipofectamine2000. In vitro assessments were then made of the ability of anti-VEGF siRNA to knock down expression of VEGF and the subsequent effect this decreased expression had on breast cancer cell apoptosis. Growth curve construction and nude mice experimentation in vivo were performed to assess the effects of VEGF silencing on tumor growth. Those cells transfected with siRNA targeting VEGF showed a 65% knockdown in VEGF expression and a marked increase in cell apoptosis. The expression of Bcl-2 protein in MCF-7 cells was decreased, the level of Bax protein was kept the same, cytochrome c was released from mitochondria into cytosol, and the cleaved Caspase-3 protein rose after siRNA transfection. The siRNA targeting human VEGF could induce apoptosis in MCF-7 cells and the mechanism of apoptosis is possibly related with changing Bcl-2/Bax expression ratio, releasing cytochrome c from mitochondria into cytosol, and up-regulation of Caspase-3 protein, but also could suppress the growth of breast cancer cells in vivo. VEGF might be a potential therapeutic target for human breast cancer.