Long non-coding RNAs (LncRNAs) represent a novel class of noncoding RNAs that are longer than 200 nucleotides without protein-coding potential and function as novel master regulators in various human diseases, including cancer. Accumulating evidence shows that lncRNAs are dysregulated and implicated in various aspects of cellular homeostasis, such as proliferation, apoptosis, mobility, invasion, metastasis, chromatin remodeling, gene transcription, and post-transcriptional processing. However, the mechanisms by which lncRNAs regulate various biological functions in human diseases have yet to be determined. HOX antisense intergenic RNA (HOTAIR) is a recently discovered lncRNA and plays a critical role in various areas of cancer, such as proliferation, survival, migration, drug resistance, and genomic stability. In this review, we briefly introduce the concept, identification, and biological functions of HOTAIR. We then describe the involvement of HOTAIR that has been associated with tumorigenesis, growth, invasion, cancer stem cell differentiation, metastasis, and drug resistance in cancer. We also discuss emerging insights into the role of HOTAIR as potential biomarkers and therapeutic targets for novel treatment paradigms in cancer.

/pdf/hotair-an-oncogenic-long-non-coding-rna-in-human-cancer-2jjkhanz7k.pdf

HOTAIR: An Oncogenic Long Non-Coding RNA in Human Cancer.

Exosomes are small endogenous membrane vesicles that can mediate cell communication by transferring genetic materials. Based on that, exosomes have always been discussed as a cargo carrier for microRNA (miRNA) transportation. Accumulating data have reported the inhibitory effects of microRNA-193a (miR-193a) on non-small cell lung cancer (NSCLC) cell progression. However, the mechanisms of miR-193a delivery to cancer cells and miR-193a in exosomes have not been explored clearly in NSCLC. Given that, this work aims to decode exosomal miR-193a in cisplatin (DDP) resistance of NSCLC cells. A549 and H1299 cell lines were screened out and their parent cells and drug-resistant cells were co-cultured with human bone marrow mesenchymal stem cells (BMSCs)-derived exosomes (BMSC-Exo) that had been transfected with miR-193a mimic or si-LRRC1 to detect the colony formation, migration, apoptosis, invasion and proliferation of NSCLC cells. In vivo experiment was conducted to verify the in vitro results. BMSC-Exo with upregulated miR-193a and downregulated LRRC1 suppressed colony formation, invasion, proliferation and migration as well as advanced apoptosis of NSCLC parent cells and drug-resistant cells. BMSC-Exo combined with upregulated miR-193a reduced tumor volume and weight in mice with NSCLC. Functional studies report that BMSC-Exo shuffle miR-193a to suppress the colony formation, invasion, migration, and proliferation as well as advance apoptosis of NSCLC DDP-resistant cells via downregulating LRRC1.

/pdf/bone-marrow-mesenchymal-stem-cells-derived-exosomal-microrna-21cevb78sa.pdf

Bone marrow mesenchymal stem cells-derived exosomal microRNA-193a reduces cisplatin resistance of non-small cell lung cancer cells via targeting LRRC1

To comprehensively assess the diagnostic performance of Vesical Imaging-Reporting and Data System (VI-RADS) score for detecting the muscle invasion of bladder cancer. PubMed, Web of Science, and Embase were searched up to November 20, 2019. QUADAS-2 tool assessed the quality of included studies. The diagnostic estimates including sensitivity, specificity, positive likelihood ratio, negative likelihood ratio, and the area under the curve (AUC) of hierarchical summary receiver operating characteristic (HSROC) were calculated. Further subgroup analysis, meta-regression and sensitivity analysis were conducted. Six studies with 1064 patients were finally included. The pooled sensitivity, specificity, and AUC value were 0.90 (95% CI 0.86–0.94), 0.86 (95% CI 0.71–0.94), and 0.93 (95% CI 0.91–0.95) for VI-RADS 3 as the cutoff value. The corresponding estimates were 0.77 (95% CI 0.65–0.86), 0.97 (95% CI 0.88–0.99), and 0.92 (95% CI 0.89–0.94) for VI-RADS 4 as the cutoff value. Meta-regression analysis revealed that study design (p value 0.01) and surgical pattern of reference standard (p value 0.02) were source of the heterogeneity of pooled sensitivity. No publication bias was observed. The VI-RADS score can provide a good predictive ability for detecting the muscle invasiveness of primary bladder cancer with VI-RADS 3 or VI-RADS 4 as the cutoff value. • VI-RADS score has high sensitivity and specificity for predicting muscle invasion.
 • The diagnostic efficiencies of VI-RADS 3 and VI-RADS 4 as the cutoff value are similar.
 • VI-RADS score could be used for detecting muscle invasion of bladder cancer in clinical practice.

Use of Vesical Imaging-Reporting and Data System (VI-RADS) for detecting the muscle invasion of bladder cancer: a diagnostic meta-analysis.

Bladder cancer (BCa) is among the ten most frequent cancers globally. It is the tumor with the highest lifetime treatment-associated costs, and among the tumors with the heaviest impacts on postoperative quality of life. The purpose of this article is to review the current applications and future perspectives of the Vesical Imaging Reporting and Data System (VI-RADS). VI-RADS is a newly developed scoring system aimed at standardization of MRI acquisition, interpretation, and reporting for BCa. An insight will be given on the BCa natural history, current MRI applications for local BCa staging with assessment of muscle invasiveness, and clinical implications of the score for disease management. Future applications include risk stratification of nonmuscle invasive BCa, surveillance, and prediction and monitoring of therapy response. LEVEL OF EVIDENCE: 3 TECHNICAL EFFICACY STAGE: 2.

/pdf/vi-rads-for-bladder-cancer-current-applications-and-future-17drglcz3w.pdf

VI-RADS for Bladder Cancer: Current Applications and Future Developments

Background Epithelial-to-mesenchymal transition (EMT) and aerobic glycolysis are fundamental processes implicated in cancer metastasis. Although increasing evidence demonstrates an association between EMT induction and enhanced aerobic glycolysis in human cancer, the mechanisms linking these two conditions in endometrial cancer (EC) cells remain poorly defined. Methods We characterized the role and molecular mechanism of the glycolytic enzyme hexokinase 2 (HK2) in mediating EMT and glycolysis and investigated how long noncoding RNA DLEU2 contributes to the stimulation of EMT and glycolysis via upregulation of HK2 expression. Results HK2 was highly expressed in EC tissues, and its expression was associated with poor overall survival. Overexpression of HK2 effectively promoted EMT phenotypes and enhanced aerobic glycolysis in EC cells via activating FAK and its downstream ERK1/2 signaling. Moreover, microRNA-455 (miR-455) served as a tumor suppressor by directly interacting with HK2 mRNA and inhibiting its expression. Furthermore, DLEU2 displayed a significantly higher expression in EC tissues, and increased DLEU2 expression was correlated with worse overall survival. DLEU2 acted as an upstream activator for HK2-induced EMT and glycolysis in EC cells through two distinct mechanisms: (i) DLEU2 induced HK2 expression by competitively binding with miR-455, and (ii) DLEU2 also interacted with EZH2 to silence a direct inhibitor of HK2, miR-181a. Conclusions This study identified DLEU2 as an upstream activator of HK2-driven EMT and glycolysis in EC cells and provided significant mechanistic insights for the potential treatment of EC.

/pdf/long-non-coding-rna-dleu2-drives-emt-and-glycolysis-in-49rk9uzoa7.pdf

Long non-coding RNA DLEU2 drives EMT and glycolysis in endometrial cancer through HK2 by competitively binding with miR-455 and by modulating the EZH2/miR-181a pathway

Though androgen deprivation therapy is the standard treatment for prostate cancer (PCa), most patients would inevitably progress to castration-resistant prostate cancer (CRPC) which is the main cause of PCa death. Therefore, the identification of novel molecular mechanism regulating cancer progression and achievement of new insight into target therapy would be necessary for improving the benefits of PCa patients. This study aims to study the function and regulatory mechanism of HOTAIR/EZH2/miR-193a feedback loop in PCa progression. MSKCC and TCGA datasets were used to identify miR-193a expression profile in PCa. Cell Counting Kit-8 (CCK-8) assays, colony formation, invasion, migration, flow cytometry, a xenograft model and Gene Set Enrichment Analysis were used to detect and analyze the biological function of miR-193a. Then, we assessed the role of HOTAIR and EZH2 in regulation of miR-193a expression by using plasmid, lentivirus and small interfering RNA (siRNA). Luciferase reporter assays and chromatin immunoprecipitation assays were performed to detect the transcriptional activation of miR-193a by EZH2 and HOTAIR. Further, qRT-PCR and luciferase reporter assays were conducted to examine the regulatory role of miR-193a controlling the HOTAIR expression in PCa. Finally, the correlation between HOTAIR, EZH2 and miR-193a expression were analyzed using In situ hybridization and immunohistochemistry. We found that miR-193a was significantly downregulated in metastatic PCa through mining MSKCC and TCGA datasets. In vitro studies revealed that miR-193a inhibited PCa cell growth, suppressed migration and invasion, and promoted apoptosis; in vivo results demonstrated that overexpression of miR-193a mediated by lentivirus dramatically reduced PCa xenograft tumor growth. Importantly, we found EZH2 coupled with HOTAIR to repress miR-193a expression through trimethylation of H3K27 at miR-193a promoter in PC3 and DU145 cells. Interestingly, further evidence illustrated that miR-193a directly targets HOTAIR showing as significantly reduced HOTAIR level in miR-193a overexpressed cells and tissues. The expression level of miR-193a was inversely associated with that of HOTAIR and EZH2 in PCa. This study firstly demonstrated that miR-193a acted as tumor suppressor in CRPC and the autoregulatory feedback loop of HOTAIR/EZH2/miR-193a served an important mechanism in PCa development. Targeting this aberrantly activated feedback loop may provide a potential therapeutic strategy.

/pdf/involvement-of-aberrantly-activated-hotair-ezh2-mir-193a-9cpw2nnh2k.pdf

Involvement of aberrantly activated HOTAIR/EZH2/miR-193a feedback loop in progression of prostate cancer.

Purpose: Evaluate the diagnostic accuracy of multi-parametric magnetic resonance imaging (mp-MRI) for local staging of bladder cancer (BCa).

Materials and Methods: The databases of PubMed, Web of Science, Wanfang, and CNKI were searched for related literatures about BCa diagnosed by mp-MRI from January 1, 2000 to April 12, 2019. The strict inclusion and exclusion criteria were set up to extract records. The Quality Assessment of Diagnostic Accuracy Studies (QUADAS)-2 was used to evaluate quality of the candidate studies. The pooled sensitivity, specificity, positive likelihood ratio (+LR), negative likelihood ratio (−LR), and diagnostic odds ratio (DOR) were calculated to assess the diagnostic authenticity of mp-MRI. The summarized receiver operating characteristic (SROC) curve corresponding with the area under the curve (AUC) were analyzed to comprehensively evacuate the diagnostic value of mp-MRI.

Results: A total of 140 studies were retrieved by computer-based searching. After quality control, 4 studies with 259 patients were enrolled for meta-analysis. The pooled results showed 0.84 of sensitivity [95% confidence interval (CI) = 0.79-0.89], 0.91 of specificity (95% CI = 0.87–0.93), 8.24 of +LR (95% CI = 4.87–13.92), 0.18 of –LR (95% CI = 0.10–0.31), 49.42 of DOR (95% CI = 19.07–128.09), and 0.946 of AUC. The Spearman correlation analysis found no threshold effect (p = 0.684). A significant heterogeneity existed among 4 included studies with sensitivity (I2 = 65.7%), specificity (I2 = 60.0%) and diagnostic OR (I2 = 67.5%). The Begg's test (p = 0.497) and the egger's test (p = 0.337) found no publication bias.

Conclusion: mp-MRI acts a good diagnostic performance for bladder cancer. It is plausible that mpMRIs can be used as an important method for bladder cancer staging.

/pdf/diagnostic-accuracy-of-multi-parametric-magnetic-resonance-3axsaxk7xi.pdf

Diagnostic Accuracy of Multi-Parametric Magnetic Resonance Imaging for Tumor Staging of Bladder Cancer: Meta-Analysis.

Human major histocompatibility complex (HLA), located on 6p21.3, encodes for genes involved in antigen processing and presentation. Loss of heterozygosity (LOH) at 6p21.3 may cause downregulated expression of HLA, thus provide tumor cells with an immune-escape tumor phenotype. In the present study, we detected HLA class I expression in gastric cancer and correlated it with LOH at 6p21.3. The expression of HLA class I antigen was analyzed by immunohistochemical procedure in 50 fresh surgically removed gastric cancers and corresponding normal tissues using 5 monoclonal antibodies (mAbs). LOH studies were detected by using 6 microsatellite markers located at 6p21.3, 1 marker located at 6q21 and 2 microsatellite markers flanking the beta2m gene. HLA class I complex was obviously downregulated in gastric cancer compared with corresponding normal tissues (t=4.00, p<0.01). The expression of beta2m gene was also downregulated in tumor, but not concordant with HLA class I surface downregulation. Out of the 50 tumors, 25 (50%) showed LOH of at least one STR marker at 6p21.3 while only 11 (22%) showed LOH of the two markers flanking the beta2m gene. The LOH frequency of D6S105, which is close to HLA-A gene, was the highest in all STR markers studied (34%). Downregulation of HLA class I expression was correlated with loss of chromosomal regions at 6p21.3 (chi-squared = 5.13, p<0.05). Our results suggested that LOH of 6p21.3 contributed to HLA class I downregulated expression in gastric cancer especially at HLA-A locus. LOH of HLA-A gene might be one of the mechanisms underlying the abnormal expression of HLA class I complex.

Loss of heterozygosity at 6p21.3 underlying HLA class I downregulation in gastric cancer.

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Involvement of aberrantly activated HOTAIR/EZH2/miR-193a feedback loop in progression of prostate cancer.

Diagnostic Accuracy of Multi-Parametric Magnetic Resonance Imaging for Tumor Staging of Bladder Cancer: Meta-Analysis.

Loss of heterozygosity at 6p21.3 underlying HLA class I downregulation in gastric cancer.