Despite promising developments of treatment, the overall outcome of gastric cancer (GC) remains poor. Current tumor markers are not ideal due to relatively low sensitivity and specificity. There is an urgent need for identifying more specific and more sensitive novel markers in the clinical management of GC. MicroRNAs (miRNAs) are non-coding RNA molecules. Recently, miRNA studies have quickly moved from basic molecular research of cancer to areas of clinical application. On the basis of recent data, the present review mainly summarizes the potential role of miRNAs as molecular biomarkers for disease susceptibility, diagnosis, prognosis and drug-response prediction in GC. This review also highlights the miRNA expression profiles in GC and their relation to cancer classification and subtype stratification. Although there are still many challenges in the research field of tumor-related miRNAs, the small molecules will definitely improve the clinical management of GC in the future.
ABSTRACT. Previous studies indicated that has an important role in the progression of Ewing's sarcoma (ES). The purpose of the current study was to examine expression changes of miR125b in the serum of ES patients and evaluate if the expression level of miR-125b could serve as a new biomarker for ES. This study was performed on patients who underwent surgical resection at our hospital between 2005 and 2013 after an initial diagnosis of ES. We measured serum miR-125b levels in 63 patients with ES and 126 healthy control patients using a real-time quantitative reverse transcriptase-PCR (qRT-PCR) method. Expression levels of serum miR-125b were distinctly decreased in ES patients when compared with healthy controls (P < 0.001). ES cases that had a poor response to chemotherapy presented a significant down-regulation of miR-125b (P = 0.001). The ROC curve showed that the serum miR-125b could serve as a valuable biomarker for differentiating ES patients from healthy controls with an AUC of 0.879 (95%CI = 0.817-0.924; P < 0.001). At a cut-off value of 2.203 for miR-125b, the sensitivity was 72.8% and the specificity was 87.2% in 19049-19056 (2015) discriminating ES from the controls. Our results indicate that serum miR125b may serve as a useful noninvasive biomarker for ES.
BackgroundGliomas account for 75% of all primary malignant brain tumors in adults and result in high mortality. Accumulated evidence has declared the minichromosome maintenance protein complex (MCM) gene family plays a critical role in modulating the cell cycle and DNA replication stress. However, the biological function and clinic characterization of nine MCM members in low-grade glioma are not yet clarified.MethodsIn this study, we utilized diverse public databases, including The Cancer Genome Atlas (TCGA), Chinese Glioma Genome Atlas (CGGA), Rembrandt, Human Protein Atlas (HPA), Linkedomics, cbioportal, Tumor and Immune System Interaction Database (TISIDB), single-sample GSEA (ssGSEA), Tumor Immune Estimation Resource (TIMER), Genomics of Drug Sensitivity in Cancer (GDSC) and Cancer Therapeutics Response Portal databases to explore the mRNA and protein expression profiles, gene mutation, clinical features, diagnosis, prognosis, signaling pathway, tumor mutational burden (TMB), immune subtype, immune cell infiltration, immune modulator and drug sensitivity of nine MCMs. Afterward, qRT-PCR was utilized to detect the expression of the MCM family in glioblastoma multiforme (GBM) cell lines. The one-, three-, or five-year survival rate was predicted by utilizing a nomogram established by cox proportional hazard regression.ResultsIn this study, we found that nine MCMs were consistently up-regulated in glioma tissues and glioma cell lines. Elevated nine MCMs expressions were significantly correlated with a higher tumor stage, isocitrate dehydrogenase (IDH) mutates, 1p/19q codeletion, histological type, and primary therapy outcome. Survival analyses showed that higher expression of MCM2-MCM8 (minichromosome maintenance protein2-8) and MCM10 (minichromosome maintenance protein 10) were linked with poor overall survival (OS) and progression-free survival (PFS) in glioma patients. On the other hand, up-regulated MCM2-MCM8 and MCM10 were significantly associated with shorter disease-specific survival (DSS) in glioma patients. Univariate and multivariate analyses revealed that MCM2 (minichromosome maintenance protein2), MCM4 (minichromosome maintenance protein 4), MCM6 (minichromosome maintenance protein 6), MCM7 (minichromosome maintenance protein 7) expression and tumor grade, 1p/19q codeletion, age, and primary therapy outcome were independent factors correlated with the clinical outcome of glioma patients. More importantly, a prognostic MCMs model constructed using the above five prognostic genes could predict the overall survival of glioma patients with medium-to-high accuracy. Furthermore, functional enrichment analysis indicated that MCMs principal participated in regulating cell cycle and DNA replication. DNA copy number variation (CNV) and DNA methylation significantly affect the expression of MCMs. Finally, we uncover that MCMs expression is highly correlated with immune cell infiltration, immune modulator, TMB, and drug sensitivity.ConclusionsIn summary, this finding confirmed that MCM4 is a potential target of precision therapy for patients with glioma.
Purpose The present study investigated the expression and function of the long noncoding RNA (lncRNA) actin filament associated protein 1 antisense RNA1 (AFAP1-AS1) related to gastric cancer (GC), based on previous results from a microarray analysis. Methods Real-time quantitative polymerase chain reaction (qPCR) was used to verify the expression of AFAP1-AS1 in 97 fresh GC tissues and paired non-GC tissues, as well as in six different GC cell lines (BGC-823, SGC-7901, MGC-803, AGS, MKN-45, and MKN-28). The expression levels were subsequently correlated with the clinicopathological features of patients. siRNA against AFAP1-AS1 was transfected into GC cell lines, and cell proliferation, migration, and invasion were detected before and after silencing of AFAP1-AS1 expression. Luciferase reporter gene analysis was used to confirm the target gene of microRNA-205-5p (miR-205-5p) in 293T cells. The potential mechanism was subsequently investigated. Results qPCR results showed that AFAP1-AS1 was significantly overexpressed in GC tumor tissues and also GC cell lines, comparing to their paired non-GC tissues. Furthermore, statistical analysis revealed that the overexpression of AFAP1-AS1 was significantly correlated with tumor size ( p =0.018) and grade of differentiation ( p =0.042). Subsequently, artificially decreasing the expression of AFAP1-AS1 with its specific siRNA dramatically inhibited the proliferation, migration and invasion of GC cell lines (SGC-7901 and BGC-823 cells). Mechanical analysis suggested that AFAP1-AS1 is involved in regulation of its maternal gene, AFAP1, at both mRNA level and protein level. Luciferase reporter gene assay indicated that lncRNA AFAP1-AS1, as a ceRNA, is able to sponge miR-205-5p. Moreover, miR-205-5p has been well demonstrated to participate in the regulation of AFAP1 expression and the phenotypes of GC cells, including proliferation, migration and invasion. Conclusion AFAP1-AS1, as a novel biomarker of GC, promotes the proliferation migration and invasion of GC cells and function as ceRNA to target AFAP1 by sponging miR-205-5p.
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