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Ferrell Weeks posted an update 6 months ago
A miR-125a-5p inhibitor restored BCYRN1 siRNA function in glioma. Conclusion The present study indicates that BCYRN1 promotes glioma cell proliferation, invasion and migration in vitro. Mechanistically, upregulated expression of BCYRN1 in glioma acts as a sponge to sequester the endogenous tumor suppressor miR-125a-5p and to further increase the expression TAZ. Our findings suggest that BCYRN1 is a novel oncogene and a new therapeutic target for glioma. © 2020 Yu et al.Background Prostate cancer (PCa) is a common malignant tumor in men. lncRNA ZFAS1 plays a carcinogenic role in many types of cancer; however, its potential role in PCa remains unclear. The current study aimed to determine the expression and function of ZFAS1 in PC. Methods The ZFAS1 expression in PC tissues and cells was determined by quantitative polymerase chain reaction (qPCR). SiZFAS1, miR-135a-5p mimic and miR-135a-5p inhibitor were transfected into PCa cells. The direct target of ZFAS1 was predicted by Starbase and verified by dual-luciferase reporter. Cell viability, proliferation, apoptosis, migration and invasion of the PCa cells were determined by cell counting kit-8, clone formation assay, flow cytometer, scratch and Transwell assay, respectively. The expression levels of related proteins and mRNAs were determined by Western blotting and qPCR. Results ZFAS1 expression was up-regulated in PCa cells and tissues. ZFAS1 could competitively bind to miR-135a-5p in PCa cells, and down-regulation of ZFAS1 inhibited cell viability, proliferation, migration, invasion of PCa cells and the occurrence of epithelial-mesenchymal transformation (EMT) and promoted apoptosis of PCa cells and increased the miR-135a-5p expression. Moreover, the function of miR-135a-5p mimic in PCa cells was consistent with ZFAS1 knockdown, while the function of miR-135a-5p inhibitor was opposite to that of miR-135a-5p mimic in PCa cells. The results showed that knocking down ZFAS1 could attenuate the effects of miR-135a-5p inhibitor on cell proliferation, invasion and EMT of PCa cells. Conclusion Knocking down ZFAS1 could inhibit the proliferation, invasion and metastasis of PCa cells through regulating miR-135a-5p expression. © 2020 Pan et al.Introduction We explored the roles of lncRNA HCP5 in non-small cell lung cancer (NSCLC). Methods Levels of HCP5 were measured by performing qPCR and data were compared between non-tumor and NSCLC tissue samples by performing a paired t-test. Expression levels of miR-320 and survivin mRNA in NSCLC tissues were also measured by performing qPCR. The effects of HCP5, miR-320 and survivin overexpression on the proliferation of H23 cells were analyzed by cell proliferation assay. Results We found that HCP5 was up-regulated in NSCLC and predicted the poor survival of NSCLC patients. HCP5 was negatively correlated with miR-320 but positively correlated with survivin in NSCLC tissues. In NSCLC cells, HCP5 overexpression led to the up-regulated survivin and down-regulated miR-320. Moreover, miR-320 overexpression failed to affect HCP5 but down-regulated survivin. Cell proliferation assay showed that HCP5 and survivin overexpression led to increased, while miR-320 overexpression led to decreased cell proliferation rate. In addition, miR-320 overexpression reduced the effects of HCP5 overexpression. Conclusion Therefore, HCP5 may stimulate the proliferation of NSCLC cells by up-regulating survivin through the down-regulation of miR-320. © 2020 Li et al.Background The aim of this study was to compare the histopathological quality and physical features of the specimen of a full-core end-cut biopsy system with that of the standard side-notch system for liver biopsies. Methods A full-core end-cut 16G biopsy device and a standard side-notch 16G needle were used to take biopsies of unclear liver lesions. Patients were randomized in two groups of 16 patients each. The primary endpoint of this prospective study was the core length measured using a dedicated microscope imaging software. Secondary endpoints were the quality of the specimen rated by an independent pathologist unaware of the device (scale from 1 to 5; with 1 as best and 5 as worst), the core diameter (determined by the microscopic imaging software) and presence of fragmentation (evaluated by the pathologist). Results For the full-core (FC) and side-notch (SN) groups, the mean core length was similar with 13,599 μm and 11,570 μm (p=0.131), respectively. The quality of the specimen was significantly better in the FC-group with an average rating of 1.68 vs 2.50 (p=0.009). The fragmentation rate in the FC-group was statistically significantly lower at 2/27 (7%) than in the SN-group at 13/33 (39%) (p=0.021). The diameter in the FC-group was 1042 μm vs 930 μm in SN-group (p=0.018). © 2020 Schaible et al.Background RP11-334E6.12 is a dysregulated long noncoding RNA (lncRNA) that has never been studied in breast cancer. The biological function and potential mechanism of RNA RP11-334E6.12 in tumorigenesis are still unknown. Methods We scanned the Cancer Genome Atlas (TCGA) database and identified RP11-334E6.12 as one of the most dysregulated lncRNAs. DSS Crosslinker research buy The level of RP11-334E6.12 was assessed in breast cancer (BC) tissue samples and BC cell lines. The survival and RP11-334E6.12 expression of patients were analysed. The biological influence of RP11-334E6.12 on BC cell lines was studied using proliferation, Transwell migration, and invasion assays. Results RP11-334E6.12 was upregulated in both the TCGA database and our own database. Moreover, survival analyses indicated that RP11-334E6.12 was related to poor overall survival. Moreover, RP11-334E6.12 promoted the proliferation, migration and invasion of BC cells. RP11-334E6.12 promotes the epithelial mesenchymal transition of BC by activating the STAT3 pathway. Conclusion Taken together, our results demonstrate that RP11-334E6.12 is associated with the progression of breast cancer. Our findings indicate that long noncoding RNA RP11-334E6.12 promotes the proliferation, migration and invasion of breast cancer cells by activating the STAT3 pathway. © 2020 Sun et al.