Predictive value of miR-9 as a potential biomarker for nasopharyngeal carcinoma metastasis.
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ABSTRACT:
SUBMITTER: Lu J
PROVIDER: S-EPMC3899774 | biostudies-literature | 2014 Jan
REPOSITORIES: biostudies-literature
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Project description:PurposeTo explore the value of MRI-based radiomics features in predicting risk in disease progression for nasopharyngeal carcinoma (NPC).Methods199 patients confirmed with NPC were retrospectively included and then divided into training and validation set using a hold-out validation (159: 40). Discriminative radiomic features were selected with a Wilcoxon signed-rank test from tumors and normal masticatory muscles of 37 NPC patients. LASSO Cox regression and Pearson correlation analysis were applied to further confirm the differential expression of the radiomic features in the training set. Using the multiple Cox regression model, we built a radiomic feature-based classifier, Rad-Score. The prognostic and predictive performance of Rad-Score was validated in the validation cohort and illustrated in all included 199 patients.ResultsWe identified 1832 differentially expressed radiomic features between tumors and normal tissue. Rad-Score was built based on one radiomic feature: CET1-w_wavelet.LLH_GLDM_Dependence-Entropy. Rad-Score showed a satisfactory performance to predict disease progression in NPC with an area under the curve (AUC) of 0.604, 0.732, 0.626 in the training, validation, and the combined cohort (all 199 patients included) respectively. Rad-Score improved risk stratification, and disease progression-free survival was significantly different between these groups in every cohort of patients (p = 0.044 or p < 0.01). Combining radiomics and clinical features, higher AUC was achieved of the prediction of 3-year disease progression-free survival (PFS) (AUC, 0.78) and 5-year disease PFS (AUC, 0.73), although there was no statistical difference.ConclusionThe radiomics classifier, Rad-Score, was proven useful for pretreatment prognosis prediction and showed potential in risk stratification for NPC.Supplementary informationThe online version contains supplementary material available at 10.1007/s12672-021-00460-3.
| S-EPMC8683387 | biostudies-literature
Project description:Our previous microarray analysis indicated that miR-34c was downregulated in nasopharyngeal carcinoma (NPC). However, little is known about the function and molecular mechanism of miR-34c in NPC. In this study, miR-34c was found to be significantly downregulated in NPC cell lines and clinical tissues. Ectopic expression of miR-34c suppressed NPC cell viability, colony formation, anchorage-independent growth, cell migration and invasion in vitro, and inhibited xenograft tumor growth and lung metastasis in vivo. MET proto-oncogene (MET) was identified as a direct target of miR-34c using luciferase reporter assays, quantitative RT-PCR, western blotting and immunofluorescent staining. Overexpression of miR-34c markedly reduced MET expression at both the mRNA and protein levels. Knockdown of MET suppressed NPC cell proliferation, migration and invasion, whereas the restoration of MET rescued the suppressive effects of miR-34c. The demethylation agent 5-aza-2'-deoxycytidine (DAC) restored the expression of miR-34c in NPC cell lines. The promoter region of miR-34c was hypermethylated in NPC cells. In conclusion, miR-34c suppresses tumor growth and metastasis in NPC by targeting MET. The newly identified miR-34c/MET pathway provides further insights into the development and progression of NPC, and may represent a novel therapeutic target for NPC treatment.
| S-EPMC4669777 | biostudies-other
Project description:BackgroundRadiomics has been widely used in the study of tumours, which has predictive and prognostic value in nasopharyngeal carcinoma (NPC). Therefore, we collected relevant literature to explore the role of current radiomics in predicting the prognosis of NPC.MethodsWe performed a systematic literature review and meta-analysis in accordance with the preferred reporting items in the systematic evaluation and meta-analysis guidelines. We included papers on radiomics published before May 5, 2024, to evaluate the predictive ability of radiomics for the prognosis of NPC. The methodological quality of the included articles was evaluated using the radiomics quality score. The area under the curve (AUC), combined sensitivity and combined specificity were used to evaluate the ability of radiomics models to predict the prognosis of NPC.ResultsA total of 20 studies met the inclusion criteria for the current systematic review, and 13 papers were included in the meta-analysis. The radiomics quality score ranged from 7 to 20 (maximum score: 36). The diagnostic test forest plots showed that the diagnostic OR of radiology was 11.04 (95% CI: 5.11-23.87), while the ORs for sensitivity and 1-specificity were 0.75 (95% CI: 0.73-0.78) and 0.74 (95% CI: 0.72-0.76), respectively. It cannot be determined whether the combined model was superior to the radiomics model for predicting the prognosis of NPC. It is unclear whether the fact that the radiomics model was composed of features extracted from MRI is due to CT. The AUC of PFS was larger than that of disease-free survival (P < .05). The overall AUC value is 0.8265.ConclusionThis study summarized all the studies that examined the predictive value of radiomics for NPC prognosis. Based on the summarized AUC values, as well as sensitivity and 1-specificity, it can be concluded that radiomics has good performance in predicting the prognosis of NPC. Radiomics models have certain advantages in predicting the effectiveness of PFS compared to predicting disease-free survival. It cannot be determined whether the combination model is superior to the radiomics model in predicting NPC prognosis, nor can it be determined whether imaging methods have differences in predictive ability. The findings confirmed and provided further evidence supporting the effectiveness of radiomics for the prediction of cancer prognosis.
| S-EPMC11365615 | biostudies-literature
Project description:ObjectivesTo determine the predictive value of pretreatment MRI texture analysis for progression-free survival (PFS) in patients with primary nasopharyngeal carcinoma (NPC).MethodsEthical approval by the institutional review board was obtained for this retrospective analysis. In 79 patients with primary NPC, texture analysis of the primary tumour was performed on pretreatment T2 and contrast-enhanced T1-weighted images (T2WIs and CE-T1WIs). The Cox proportional hazards model was used to determine the association of texture features, tumour volume and the tumour-node-metastasis (TNM) stage with PFS. Survival curves were plotted using the Kaplan-Meier method. The prognostic performance was evaluated with the receiver operating characteristic (ROC) analyses and C-index.ResultsTumour volume (hazard ratio, 1.054; 95% confidence interval [CI], 1.016-1.093) and CE-T1WI-based uniformity (hazard ratio, 0; 95% CI, 0-0.001) were identified as independent predictors for PFS (p < 0.05). Kaplan-Meier analysis showed that smaller tumour volume (less than the cut-off value, 11.699 cm3) and higher CE-T1WI-based uniformity (greater than the cut-off value, 0.856) were associated with improved PFS (p < 0.05). The combination of CE-T1WI-based uniformity with tumour volume and the overall stage predicted PFS better (area under the curve [AUC], 0.825; Cindex, 0.794) than the tumour volume (AUC, 0.659; C-index, 0.616) or the overall stage (AUC, 0.636; C-index, 0.627) did (p < 0.05).ConclusionsA texture parameter of pretreatment CE-T1WI-based uniformity improves the prediction of PFS in NPC patients.Key points• Higher CE-T1WI-based uniformity and smaller tumour volume are predictive of improved PFS in NPC patients. • The combination of CE-T1WI-based uniformity with tumour volume and the overall stage has a better predictive ability for PFS than the tumour volume or the overall stage alone. • Pretreatment MRI texture analysis has a prognostic value for NPC patients.
| S-EPMC6610272 | biostudies-literature
Project description:This study explored the changes and predictive value of miR-34a in nasopharyngeal carcinoma (NPC) after concurrent chemoradiotherapy (CCRT), and its association with cognitive function. Fifty NPC patients admitted to Shunde Hospital, and another fifty healthy individuals were assigned into treated group and control group, respectively. Patients in the treated group received 3 courses of CCRT. The relative expression of miR-34a in the two groups was detected, and the cognitive function of patients was assessed. Diagnostic and predictive values of miR-34a in advanced NPC were analyzed. The expression of miR-34a in the control group was significantly higher than that in the treated group (t=13.364, P<0.001), with an area under the curve (AUC) of 0.979. The expression of miR-34a was significantly upregulated after treatment (t=4.559, P<0.001). After treatment, there were 32 complete remission (CR) patients and 18 partial remission (PR) patients. According to efficacy, CR patients were classified as significant group and PR patients as general group. The expression of miR-34a in the significant group was higher than that in the general group before treatment (t=4.704, P<0.001), with an AUC of 0.852. The Montreal Cognitive Assessment (MoCA) score was significantly decreased after treatment (t=13.042, P<0.001). The expression of miR-34a was positively correlated with the MoCA score after treatment, that is, MoCA score gradually increased with the upregulation of miR-34a expression (r=0.379, P=0.006). There is a positive correlation between miR-34a and cognitive function of patients. Moreover, the expression of miR-34a can be used as a potential predictor of the efficacy of CCRT in patients with NPC.
| S-EPMC7471644 | biostudies-literature
Project description:Metastasis is the major reason of treatment failure in nasopharyngeal carcinoma. miRNAs have been identified to regulate tumor metastasis. We aimed to identify metastasis-associated miRNAs in nasopharyngeal carcinoma.
2020-02-24 | GSE137312 | GEO
Project description:Pancreatic adenocarcinoma is one of the most lethal diseases with a 5-year survival rate of about 8%. ASXL2 is an epigenetic regulator associated with various tumors including colorectal cancer, breast cancer, and myeloid leukemia. However, the role of ASXL2 in pancreatic cancer remains unclear. This is the first research focusing on the prognostic value of ASXL2 in pancreatic cancer. In this research, we aimed to explore the correlation between ASXL2 and the prognosis, as well as other features in PAAD. We obtained gene expression profiles of PAAD and normal tissues from TCGA, GEO, and Xena databases. TIMER and CIBERSORT algorithms were employed to investigate the effect of ASXL2 on tumor microenvironment. GSEA along with GO and KEGG enrichment analyses were conducted to uncover the biological functions of ASXL2. The response to various chemotherapeutic drugs was estimated by algorithms in R package "pRRophetic", while the sensitivity to immunotherapy was quantified by TIDE score. We found that ASXL2 was upregulated in the PAAD samples and elevated expression of ASXL2 was linked to poor overall survival. ASXL2 DNA methylation contributed to ASXL2 expression. Functional annotation indicated that ASXL2 was mainly involved in inflammatory response and epithelial mesenchymal transition. Patients with high ASXL2 expression were more likely to benefit from immune checkpoint blockade, gemcitabine, and mitomycin-C. Finally, external datasets and biospecimens were used and the results further validated the aberrant expression of ASXL2 in PAAD samples. In summary, our results highlight that ASXL2 is a potential prognostic and predictive biomarker in pancreatic cancer.
| S-EPMC8531590 | biostudies-literature
Project description:BACKGROUND:The molecular mechanisms underlying dysregulation of microRNAs have been documented in nasopharyngeal carcinoma (NPC). Our previous study demonstrated that plasma miR-124 was down-regulated in NPC using microarray analysis and quantitative PCR validation. Though growing studies showed that down-regulated miR-124 was closely related to tumourigenesis in various types of cancers, the role of miR-124 in NPC remains largely unknown. METHODS:The expression level of miR-124 was evaluated in NPC cell lines and patient specimens using quantitative reverse transcription-PCR (Real-time qPCR). The clinicopathological significance of the resultant data was later analyzed. Then, we explored the role of miR-124 in NPC tumorigenesis by in vitro and in vivo experiments. Homo sapiens forkhead box Q1 (Foxq1) was confirmed as a novel direct target gene of miR-124 by the dual-luciferase assay and western bolt. RESULTS:We found that miR-124 was commonly down-regulated in NPC specimens and NPC cell lines. The expression of miR-124 was inversely correlation with clinical stages and marked on T stages. Then, the ectopic expression of miR-124 dramatically inhibited cell proliferation, colony formation, migration and invasion in vitro, as well as tumor growth and metastasis in vivo. Furthermore, we identified Foxq1 as a novel direct target of miR-124. Functional studies showed that knockdown of Foxq1 inhibited cell growth, migration and invasion, whereas Foxq1 overexpression partially rescued the suppressive effect of miR-124 in NPC. In clinical specimens, Foxq1 was commonly up-regulated in NPC, and the level increased with clinical stages and T stages. Additionally, the level of Foxq1 was inversely correlated with miR-124. CONCLUSIONS:Our results demonstrate that miR-124 functions as a tumor-suppressive microRNA in NPC, and that its suppressive effects are mediated chiefly by repressing Foxq1 expression. MiR-124 could serve as an independent biomarker to identify patients with different clinical characteristics. Therefore, our findings provide valuable clues toward the understanding the of mechanisms of NPC pathogenesis and provide an opportunity to develop new effective clinical therapies in the future.
| S-EPMC4267157 | biostudies-literature
Project description:BACKGROUND: Mitochondrial proteomic alterations of nasopharyngeal carcinoma metastasis remain unknown. Our purpose is to screen mitochondrial proteins for the elucidation of the molecular mechanisms of nasopharyngeal carcinoma metastasis and the discovery of metastasis-related biomarkers. METHODS: Mitochondria were isolated from nasopharyngeal carcinoma metastatic (5-8F) and nonmetastatic (6-10B) cell lines, respectively. After characterization of isolated mitochondria, mitochondrial differentially expressed proteins (DEPs) were quantified by two-dimensional difference in-gel electrophoresis (2D-DIGE), and identified by peptide mass fingerprint (PMF) and tandem mass spectrometry (MS/MS). A functional enrichment analysis and a protein-protein interaction sub-network analysis for DEPs were carried out with bioinformatics. Furthermore, siRNAs transient transfections were used to suppress expressions of some up-regulated DEPs in metastatic cells (5-8F), followed by Transwell Migration assay. RESULTS: Sixteen mitochondrial DEPs including PRDX3 and SOD2 were identified. Those 5-8F cells with suppression of PRDX3 showed an increased mobility potential. The functional enrichment analyses of DEPs discovered five significant biological processes including cellular response to reactive oxygen species, hydrogen peroxide metabolic process, regulation of mitochondrial membrane potential, cell redox homeostasis and oxidation reduction, and five significant molecular functions including oxidoreductase activity, caspase inhibitor activity, peroxiredoxin activity, porin activity and antioxidant activity. A protein-protein interaction sub-network of DEPs was generated with literature data. Ten mitochondrial DEPs including PRDX3, PRDX6, SOD2, ECH1, SERPINB5, COX5A, PDIA5, EIF5A, IDH3B, and PSMC4 were rationalized in the tumor-stroma co-evolution model that mitochondrial oxidative stress directly contributes to tumor metastasis. CONCLUSIONS: Sixteen mitochondrial DEPs were identified with mass spectrometry and ten of them were rationalized in the tumor-stroma co-evolution model. Those 5-8F cells with suppression of PRDX3 showed an increased mobility potential. These data suggest that those mitochondrial DEPs are potential biomarkers for NPC metastasis, and their dysregulation would play important roles in mitochondria oxidative stress-mediated NPC metastatic process.
| S-EPMC3539862 | biostudies-other
Project description:Nasopharyngeal carcinoma (NPC) has insidious onset, late clinical diagnosis and high recurrence rate, which leads to poor quality of patient life. Therefore, it is necessary to further explore the pathogenesis and therapy targets of NPC. BUB1 mitotic checkpoint serine/threonine kinase B (BUB1B) was found to be up-regulated in a variety of cancers, but only two previous study showed that BUB1B was overexpressed in NPC and the sample size was small. The clinical role of BUB1B expression and its underlying mechanism in NPC require more in-depth research. Immunohistochemical samples and public RNA-seq data indicated that BUB1B protein and mRNA expression levels were up-regulated in NPC, and summary receiver operating characteristic curve indicated that BUB1B expression level had a strong ability to distinguish NPC tissues from non-NPC tissues. Gene ontology and Kyoto Encyclopedia of genes and genomes were performed and revealed that BUB1B and its related genes were mainly involved in cell cycle and DNA replication. Protein- Protein Interaction were built to interpret the BUB1B molecular mechanism. Histone deacetylase 2 (HDAC2) could be the upstream regulation factor of BUB1B, which was verified by Chromatin Immunoprecipitation Sequencing samples. In summary, BUB1B was highly expressed in NPC, and HDAC2 may affect cell cycle by regulating BUB1B to promote cancer progression.
| S-EPMC9798722 | biostudies-literature