Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0178874 (tumor progression)
 40,807 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recent studies have demonstrated that the chemokine CCL20 and its receptor CCR6 may be involved in tumorigenesis, tumor progression and metastatic spread of various human malignancies. The aim of this study was to investigate the clinicopathological significance and prognostic value of CCL20 and CCR6 expression in human malignant glioma. CCL20 and CCR6 expression in human gliomas and nonneoplastic brain tissues was measured by immunohistochemistry. The association of CCL20 and CCR6 expression with clinicopathological factors or prognosis in glioma patients was statistically analyzed. The expression levels of CCL20 and CCR6 proteins were both up-regulated in glioma tissues. There was a significantly positive correlation between the expression of the two markers (r = 0.88; P < 0.001). In addition, the overexpressions of CCL20 and CCR6 were both detected in high-grade glioma tissues compared with those in low-grade tissues and increased with ascending tumor World Health Organization (WHO) grades (P = 0.006 and 0.008, respectively). The increased expressions of CCL20 and CCR6 proteins were also significantly correlated with low Karnofsky performance score (both P = 0.01). Moreover, univariate analysis found that CCL20 expression (P = 0.002), CCR6 expression (P = 0.002) and CCL20/CCR6 co-expression (P < 0.001) were all significantly associated with poor prognosis. In particular, glioma patients with CCL20/CCR6 co-expression have the shortest overall survival. Multivariate analysis further identified the expression levels of CCL20 and CCR6 to be independent prognostic factors. Our data suggest for the first time that CCL20 and CCR6 might play an important role in the regulation of aggressiveness in human gliomas. The up-regulation of CCL20 and CCR6 might be closely associated with poor clinical outcome of patients with gliomas.
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PMID:Overexpression of CCL20 and its receptor CCR6 predicts poor clinical prognosis in human gliomas. 2292 20

F box only protein 8 (FBX8) is a novel component of F-box proteins which involved in the ubiquitin-dependent proteolytic pathway. Recent studies have revealed that FBX8 was unregulated in tumor cells and was closely associated with tumor progression and metastasis of other cancer, but little research has been done yet to test its usefulness as a prognostic marker in human glioma. In the present study, we investigated the expression of FBX8 in glioma tissues using immunohistochemical analysis and evaluated its prognostic significance in glioma. We found that 44/77 (57.14%) gilomas had positive expression of FBX8, while 65/77 (84.42%) normal brain tissue had positive expression of FBX8. The expression level of FBX8 was remarkably down-regulated in glioma tissues compared with normal brain tissues (P < 0.001). The down-expression of FBX8 in tumor cells was strongly correlated with tumor grade of patients with glioma (P < 0.05). Patients with lower expression of FBX8 protein had shorter overall survival time than those with higher level expression of FBX8 (P < 0.05). Multivariate analysis showed that FBX8 down-expression was an independent prognostic indicator for glioma patient's survival. Our results suggest that a potential application of FBX8 in prognosis prediction and therapeutic application in glioma.
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PMID:Down-expression of F box only protein 8 correlates with tumor grade and poor prognosis in human glioma. 2555 Aug 53

Poor prognosis of glioma is due to the characteristics of high invasiveness. Recently, it was demonstrated that Gab2 was over-expressed and related to cellular migration and invasion in glioma, however, the mechanisms of regulation are still unknown. A better understanding of molecular events key to the carcinogenesis and tumor progression may facilitate development of new therapeutic targets and anti-glioma strategies. This study is the first to focus on miR125a-5p, which was predicted to regulate Gab2 with directly targeting the 3' un-translated region (3'UTR) of Gab2 and could inhibit migration and invasion of glioma cells by mediating Gab2 to affect cytoskeleton rearrangement and matrix metalloproteinases expression. Interestingly, further evaluation revealed that the miR125a-5p promoter was hypermethylated and that attenuating promoter methylation was sufficient to up-regulate miR125a-5p expression in glioma cells. Additionally, we reported that miR125a-5p was down-regulated in glioma as well as statistical analysis suggested that its expression level correlated with the World Health Organization grades of glioma (P < 0.05) and that patients with a low miR125a-5p level exhibited shorter survival time (P < 0.05). Taken together, these results reveal that miR125a-5p represents potential therapeutic targets in glioma by modulating Gab2.
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PMID:MiR125a-5p acting as a novel Gab2 suppressor inhibits invasion of glioma. 2559 21

Glioma is the most common and malignant brain tumor with extremely poor prognosis. It is crucial to understand the molecular characteristics of glioma and find out more effective therapeutic targets for the treatment of glioma. USP17 is a novel deubiquitinating enzyme that is differentially expressed in certain types of solid tumor. Our present study investigated the pathological functions and clinical significance of USP17 in glioma for the first time. We found that USP17 was down-regulated in glioma tissue compared with normal tissues. Overexpression of USP17 in glioma cells reduced their tumorigenesis and proliferation ability through reducing Ras and Myc protein levels. Subsequent in vivo experiments showed that overexpression of USP17 suppressed tumor progression in an orthotopic glioma models. Further, study of a cohort of 104 patients with stage I-IV glioma showed that USP17 expression was negatively associated with the WHO grade (p<0.001). USP17 was more highly expressed in low grade (I+II) glioma than high-grade (III+IV) glioma (p<0.001). Taken together, our results indicate that USP17 might play important functions in glioma through suppressing glioma tumorigenesis and proliferation.
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PMID:Expression and functional implications of USP17 in glioma. 2677 24

Acylglycerol kinase (AGK) regulates various cellular processes involved into tumorigenesis and tumor progression. To investigate involvement of AGK in human gliomas, here, quantitative real-time polymerase chain reaction, Western blot, and immunohistochemistry analyses were performed to respectively detect the expression of AGK mRNA and protein in glioma and nonneoplastic brain tissue specimens. Then, the associations of AGK expression with various clinicopathological characteristics and patients' prognosis were statistically evaluated. Moreover, the effects of siRNA-mediated AGK knockdown on glioma cell proliferation, migration, and invasion were respectively assessed via Cell Counting Kit-8 and Transwell assays in vitro. As a result, AGK expression, at both mRNA and protein levels, were markedly up-regulated in glioma tissues compared with nonneoplastic brain tissues (both P < .001). In addition, high AGK expression was significantly associated with the grade of malignancy and poor prognosis in glioma patients (all P < .05). Importantly, Cox regression model of multivariate analysis identified AGK expression as an independent prognostic factor for glioma patients (P = .03). Furthermore, silencing the expression of AGK dramatically suppressed cell proliferation, migration, and invasion of glioma cells in vitro (all P < .05). In conclusion, AGK up-regulation may be involved into glioma development and progression, highlighting its prognostic value for the treatment of patients with this malignancy. Further loss-of-function experiments suggest that AGK might play an important role in the viability and motility of glioma cells, implying its potentials as an attractive therapeutic target for this tumor.
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PMID:Acylglycerol kinase functions as an oncogene and an unfavorable prognostic marker of human gliomas. 2757 11

Long non-coding RNA (lncRNA) X inactivate-specific transcript (XIST) acts as an important regulator in tumor progression. However, its expression and the underlying mechanism in glioma remain unclear. The aim of this study was to explore the potential function of XIST in glioma progression. In the present study, our data showed that the expression of XIST was significantly up-regulated in glioma tissues and enhanced the proliferation of glioma cells. The expression of miR-137 was significantly decreased in glioma tissues. Further correlation analysis demonstrated that there was a negative correlation between XIST expression and miR-137 expression. Bioinformatics prediction and luciferase reporter assays demonstrated that miR-137 could directly bind to XIST and negatively regulated the expression of miR-137. Additionally, our data further showed that XIST could up-regulate the expression of miR-137 targeted gene Rac1 through acting as an endogenous sponge of miR-137. In addition, we found that Rac1 inhibition or miR-137 overexpression could suppress glioma cells proliferation induced by XIST overexpression. Thus, a novel XIST-miR-137-Rac1 pathway regulatory axis in glioma pathogenesis was revealed in the present study. Overall, our study indicated that XIST could be a potential therapeutic target in the treatment of glioma.
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PMID:Long non-coding RNA XIST exerts oncogenic functions in human glioma by targeting miR-137. 2846 89

Long non-coding RNAs (lncRNAs) are proved as important regulators in many diseases, including multiple cancers. HOXA11antisense RNA (HOXA11-AS) is a novel identified lncRNA associated with cancer progression. However, the role of HOXA11-AS in glioma remains poorly understood and needs to be elucidated. The purpose of this study is to investigate the role and regulating mechanism of HOXA11-AS on gliomagenesis. Expression of HOXA11-AS was significantly up-regulated in glioma tissue and cell lines compared to the adjacent normal tissue and cells. Moreover, patients with high HOXA11-AS expression had a shorter survival time and poorer prognosis than that of lower expression. Loss-of-function experiments revealed that HOXA11-AS knockdown inhibited the proliferation, induced cell cycle arrest at G0/G1 phase and enhanced the apoptosis. Bioinformatics prediction forecast that miR-140-5p directly targeted HOXA11-AS at 3'-UTR, which was confirmed by luciferase reporter assay. In vitro rescue experiment assays, miR-140-5p inhibitor transfection could reverse the function of HOXA11-AS knockdown on the proliferation, cell cycle arrest and apoptosis. Together, present study illustrates that the pathway of HOXA11-AS sponging miR-140-5p might play a vital regulating role in the development and progression of glioma.
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PMID:WITHDRAWN: Knockdown of LncRNA HOXA11 Antisense Promotes Glioma Cell Apoptosis Via Sponging MiR-140-5p. 2865 5

Increasing evidence suggests the involvement of long noncoding RNAs (lncRNAs) in various biological process including cancer progression and drug resistance. LncRNA HOXD cluster antisense RNA 1 (HOXD-AS1) had been demonstrated to act as an oncogenic gene, contributing to the development and progression of several cancers. However, its functional role and molecular mechanism underlying glioma progression and cisplatin (DDP) resistance has not been well elucidated. In this study, we found that HOXD-AS1 was up-regulated in glioma tissues and cells and negatively correlated with survival time. HOXD-AS1 knockdown suppressed proliferation, migration and invasion as well as enhanced DDP sensitivity of glioma cells. Moreover, HOXD-AS1 could function as a miR-204 sponge in glioma cells. Overexpression of miR-204 could mimic the functional role of down-regulated HOXD-AS1 in glioma cells. Furthermore, miR-204 inhibition reversed the effect of HOXD-AS1 knockdown on cancer progression and DDP sensitivity of glioma cells. In conclusion, knockdown of HOXD-AS1 suppressed proliferation, migration and invasion and enhanced DDP sensitivity of glioma cells through sequestering miR-204, providing a promising therapeutic target for glioma patients.
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PMID:Knockdown of lncRNA HOXD-AS1 suppresses proliferation, migration and invasion and enhances cisplatin sensitivity of glioma cells by sponging miR-204. 3078 27

miR-517a has been reported to act as an oncogenic miRNA in human hepatocellular carcinoma and lung cancer. However, the roles and underlying molecular mechanism of miR-517a in glioma remain unclear. In the present study, the expression of miR-517a in clinical glioma tissues and glioma cell lines was examined by quantitative real-time PCR (qRT-PCR). Transfected with knockdown or forced expression of miR-517a, the effects of miR-517a on cell proliferation, migration, and invasion were detected through in vitro and in vivo tumorigenesis assays. Here, we report that miR-517a expression was up-regulated in glioma tissues when compared with normal brain tissues, and up-regulation of miR-517a level is tightly correlated with the status of pathology classification of glioma. A functional assay found that overexpression of miR-517a in glioma cells markedly promoted or suppressed cell proliferation, colony formation, migration and invasion, respectively. Moreover, we revealed that the knockdown of miR-517a dramatically suppressed glioma cell growth, migration, and invasion in vitro and in vivo Furthermore, we found that knockdown of miR-517a significantly induced apoptosis. Therefore, miR-517a acts an oncogenic miRNA that promotes tumor progression in glioma, and thus may become a promising therapeutic candidate for glioma.
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PMID:miR-517a is up-regulated in glioma and promotes glioma tumorigenesis in vitro and in vivo. 3096 71

Epithelial-mesenchymal transition (EMT) plays a pivotal role in cancer progression. Hsa-miR-205 is considered one of the fundamental regulators of EMT. In the present study, we found that miR-205 was down-regulated in glioma tissues and human glioma cells U87 and U251. Meanwhile, miR-205 overexpression enhanced E-cadherin, reduced mesenchymal markers, and decreased cell proliferation, migration, and invasion in vitro. In vivo, miR-205 suppressed tumor growth. Additionally, HOXD9 was confirmed as a direct target of miR-205. Suppression of HOXD9 by miR-205 was demonstrated by luciferase reporter assay, quantitative real time-PCR analysis, and western blot. Moreover, we observed a negative correlation between miR-205 and HOXD9 in human glioma tissues. In summary, our findings demonstrated that miR-205 suppresses glioma tumor growth, invasion, and reverses EMT through down-regulating its target HOXD9.
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PMID:MiR-205 suppresses epithelial-mesenchymal transition and inhibits tumor growth of human glioma through down-regulation of HOXD9. 3099 94


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