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Background New evidence from clinical and fundamental researches suggests that SNHG7 is involved in the occurrence and development of carcinomas. And the increased levels of SNHG7 are associated with poor prognosis in various kinds of tumors. However, the small sample size was the limitation for the prognostic value of SNHG7 in clinical application. The aim of the present meta-analysis was to conduct a qualitative analysis to explore the prognostic value of SNHG7 in various cancers. Methods Articles related to the SNHG7 as a prognostic biomarker for cancer patients, were comprehensive searched in several electronic databases. The enrolled articles were qualified via the preferred reporting items for systematic reviews and meta-analysis of observational studies in epidemiology checklists. Additionally, an online database based on The Cancer Genome Atlas (TCGA) was further used to validate our results. Results We analyzed 2418 cancer patients that met the specified criteria. The present research indicated that an elevated SNHG7 expression level was significantly associated with unfavorable overall survival (OS) (HR = 2.45, 95% CI: 2.12–2.85, p p p p p p Conclusions The present analysis suggests that elevated SNHG7 is significantly associated with unfavorable OS, tumor progression, LNM and DM in various carcinomas, and may be served as a promising biomarker to guide therapy for cancer patients.

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 P 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.

// Jia Liu 1, * , Jieru Lin 2, * , Yingqi Li 4 , Yunyuan Zhang 3 and Xian Chen 3 1 Department of Pharmacy, Guiyang Maternal and Child Health Care Hospital, Guiyang 550003, China 2 Department of Respiratory and Critical Care Medicine, Guizhou Provincial People's Hospital, Guiyang 550002, China 3 Department of Clinical Laboratory, The Affiliated Hospital of Qingdao University, Qingdao 266003, China 4 Department of Ophthalmology, The Affiliated Hospital of Guizhou Medical University, Guiyang 550004, China * These authors contributed equally to this work Correspondence to: Xian Chen, email: cxkakicoco2014@163.com Keywords: cancer, prognosis, long non-coding RNA, taurine upregulated gene 1 Received: February 25, 2017 Accepted: April 29, 2017 Published: May 13, 2017 ABSTRACT LncRNA TUG1 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, this meta analysis was conducted to analyze available data to delineate the potential clinical application of lncRNA TUG1 on cancer prognosis, lymph node metastasis and tumor progression. 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. The hazard ratios (HR) with 95% confidence interval (95% CI) were calculated to assess the strength of the association. Eight studies with a total of 840 cancer patients were included in the present meta analysis. The results indicated that elevated lncRNA TUG1 significantly predicted unfavorable overall survival (OS) (HR = 2.06, 95% CI: 1.23–3.45, P = 0.006), but failed to show incline to lymph node metastasis (HR: 1.16, 95% CI: 0.82–1.62, P = 0.40) and disease progression (III/IV vs. I/II: HR 1.16, 95% CI: 0.74–1.81, P = 0.52). In stratified analyses, a significantly unfavorable OS associated with elevated lncRNA TUG1 was observed in both bladder cancer (HR = 2.98, 95% CI: 1.84–4.83, P < 0.0001) and other system cancer (HR = 2.63, 95% CI: 1.42–4.87, P = 0.002), but not respiratory system cancer (HR = 0.93, 95% CI: 0.30–2.82, P = 0.895). The results indicated that increased lncRNA TUG1 was an independent prognostic biomarker for unfavorable OS but may not susceptible to lymph node metastasis and tumor progression in cancer patients.

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

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

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.

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.

Background Increasing evidence revealed that high expression level of lncRNA SNHG1 was associated with the unfavorable prognosis of cancer and maybe used as a valuable biomarker for cancer patients. The present meta->analysis is to analyze existing data to reveal potential clinical application of SNHG1 on cancer prognosis and tumor progression. All of the included studies were collected through a variety of retrieval strategies. And the articles were qualified by MOOSE and PRISMA checklists. Methods Up to Mar 20, 2018, literature collection was performed by comprehensive search through electronic databases, including the Cochrane library, PubMed, Embase, Web of science, Springer, Science direct, and three Chinese databases: CNKI, Weipu, and Wanfang. We analyzed 14 studies that met the criteria, and concluded that the increased SHNG1 level was correlated with poor OS and tumor progression. Results The combined results indicated that elevated SNHG1 expression level was significantly associated with poor OS (HR = 2.06, 95% CI: 1.69–2.52, P

Bone morphogenetic proteins (BMPs) are members of the TGF-β superfamily signaling factors. Expression of several BMPs (BMP2, BMP4, and BMP7) is correlated to poor prognosis in gastric cancer patients. The function of BMP9, the latest discovered and most powerful osteogenetic factor, in gastric cancer is relatively unclear. In this report, we investigated the expression, function and underlying molecular mechanisms of BMP9 in gastric cancer. The results show that BMP9 expression was markedly decreased in gastric cancer tissues and cell lines. Enforced BMP9 expression in the gastric cancer cell lines SGC-7901 and MNK-45 increased apoptosis and reduced viability and migration. The in vivo function of BMP9 was evaluated in a xenograft mouse model. Tumors derived from SGC-7901 cells with enforced BMP9 expression (SGC-7901/BMP9) showed significantly reduced size and weight compared to that from control cells. Enforced BMP9 expression resulted in decreased Akt activity shown as lower levels of phosphorylation at Ser473 and Thr308 in Akt. The PI3K/Akt inhibitor LY294002 potentiated BMP9's viability and migration suppression, and apoptosis induction, which was associated with reduced expression of snail and VEGF and increased expression of E-cadherin. In addition, tumors derived from SGC-7901/BMP9 showed reduced Akt activity and VEGF expression, and increased E-cadherin expression. Therefore, our studies reveal for the first time that inhibition of the PI3K-Akt pathway is involved in the tumor suppressor effects of BMP9 in gastric cancer.

Hepatocellular carcinoma (HCC) is associated with hepatitis B virus (HBV) infection. Myeloid-specific S100 proteins (S100s), namely, S100A8, S100A9 and S100A12, have been recently recognized as newly discovered damage-associated molecular patterns (DAMPs) that are correlated with progression in pathogen of infectious diseases. However, whether S100s are regulated by HBV and involved in HBV-related hepatocarcinogenesis are still unclear. Here, we found that all expression levels of myeloid-specific S100s (S100A8, S100A9 and S10012) were elevated in serum and tissue samples from HCC patients. Expression of S100A9 but not S100A8 and S10012 were also higher in blood serum and tissue samples from HBV-positive HCC patients than that in HBV-negative HCC patients. High levels of intracellular and extracellular S100A9 were also confirmed in HepG2 cells expressing 1.3-fold HBV genome or HBV-encoded X protein (HBx) as well as in a stable HBV-producing cell line HepG2.2.15. HBx was shown to facilitate translocation of NF-κB from the cytoplasm to the nucleus, and NF-κB bound to the promoter of S100A9 to enhance its transcription. Silencing S100A9 expression partially blocked HBx-induced growth and metastasis of HepG2 cells both in vitro and in vivo. Further, serum S100A9 levels were found to correlate with TNM stage, extrahepatic metastasis status and HBV DNA load in HBV-related HCC and also had a better diagnostic value for identifying extrahepatic metastasis. Our these data demonstrate that S100A9 plays a pivotal role in HBx-induced growth and metastasis of HCC and may serve as a potential diagnostic marker for extrahepatic metastasis.

Colorectal cancer (CRC) is one of the most deadly cancers worldwide. Significant progress has been made in understanding the molecular pathogenesis of CRC, which has led to successful early diagnosis, surgical intervention and combination chemotherapy. However, limited therapeutic options are available for metastatic and/or drug-resistant CRC. While the aberrantly activated Wnt/β-catenin pathway plays a critical initiating role in CRC development, disruption of the bone morphogenetic protein (BMP) pathway causes juvenile polyposis syndrome, suggesting that BMP signaling may play a role in CRC development. However, conflicting results have been reported concerning the possible roles of BMP signaling in sporadic colon cancer. Here, we investigated the effect of BMP2 on the proliferation, migration, invasiveness and tumor growth capability of human CRC cells. Using an adenovirus vector that overexpresses BMP2 and the piggyBac transposon-mediated stable BMP2 overexpression CRC line, we found that exogenous BMP2 effectively inhibited HCT116 cell proliferation and colony formation. BMP2 was shown to suppress colon cancer cell migration and invasiveness. Under a low serum culture condition, forced expression of BMP2 induced a significantly increased level of apoptosis in HCT116 cells. Using a xenograft tumor model, we found that forced expression of BMP2 in HCT116 cells suppressed tumor growth, accompanied by decreased cell proliferation activity. Taken together, our results strongly suggest that BMP2 plays an important inhibitory role in governing the proliferation and aggressive features of human CRC cells.

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

Numerous individual studies evaluating the relationship between CD44V6 over-expression and prognostic impact in patients with osteosarcoma (OS) have yielded in conclusive results. This meta-analysis aimed to determine the value of cell adhesion molecule CD44V6 in prognosis of OS by conducting a systematic review and meta-analysis. A comprehensive search was conducted using PubMed (medline), Embase, ISI Web of Knowledge, Springer, the Cochrane Library, Scopus, BioMed Central, ScienceDirect, Wanfang, Weipu, and China National Knowledge Internet (CNKI) databases from inception through May 26, 2015. All available articles written in English or Chinese that investigated the expression of CD44V6 and the prognosis of OS were included. The quantity of the studies was evaluated according to the critical review checklist of the Dutch Cochrane Centre proposed by MOOSE. Finally, a total of eight studies with 486 OS patients were involved and the results indicated that the positive expression of CD44V6 predicts neoplasm metastasis (RR = 1.76, 95 % CI 1.38–2.25, p

Background and Objective S100A8 and S100A9, two members of the S100 protein family, have been reported in association with the tumor cell differentiation and tumor progression. Previous study has showed that their expression in stromal cells of colorectal carcinoma (CRC) is associated with tumor size. Here, we investigated the clinical significances of S100A8 and S100A9 in tumor cells of CRC and their underlying molecular mechanisms. Methods Expression of S100A8 and S100A9 in colorectal carcinoma and matching distal normal tissues were measured by reverse transcriptase polymerase chain reaction (RT-PCR), immunohistochemistry and western blot. CRC cell lines treated with the recombinant S100A8 and S100A9 proteins were used to analyze the roles and molecular mechanisms of the two proteins in CRC in vitro. Results S100A8 and S100A9 were elevated in more than 50% of CRC tissues and their expression in tumor cells was associated with differentiation, Dukes stage and lymph node metastasis. The CRC cell lines treatment with recombinant S100A8 and S100A9 proteins promoted the viability and migration of CRC cells. Furthermore, the two recombinant proteins also resulted in the increased levels of β-catenin and its target genes c-myc and MMP7. β-catenin over-expression in CRC cells by Adβ-catenin increased cell viability and migration. β-catenin knock-down by Adsiβ-catenin reduced cell viability and migration. Furthermore, β-catenin knockdown also partially abolished the promotive effects of recombinant S100A8 and S100A9 proteins on the viability and migration of CRC cells. Conclusions Our work demonstrated that S100A8 and S100A9 are linked to the CRC progression, and one of the underlying molecular mechanisms is that extracellular S100A8 and S100A9 proteins contribute to colorectal carcinoma cell survival and migration via Wnt/β-catenin pathway.