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Objective Circular RNA is a newly discovered non-coding RNA. It plays an important role in regulating gene expression, and may take part in tumor progression. This study aimed to investigate the functions of hsa_circ_0008792 in osteosarcoma regulation. Methods We identified a circular RNA, hsa_circ_0008792, by using bioinformatics to analyze the GSE96962 dataset. The capacities of migration and invasion were assessed by wound-healing assay and transwell Matrigel assay. The ratios of G0/G1, S, and G2/M phases in cell cycle and apoptosis were measured using flow cytometry. Results Hsa_circ_0008792 is expressed at low levels in osteosarcoma cells, and up-regulation of hsa_circ_0008792 could suppress osteosarcoma cell migration and invasion and promote apoptosis. This regulation is mediated by hsa-miR-711/ZFP1. The expression level of hsa_circ_0008792 showed no influence on cell cycle of osteosarcoma cells. Conclusion Osteosarcoma is suppressed by hsa_circ_0008792/hsa-miR-711/ZFP1 axis. © 2020 Chen et al.Background Gastric cancer (GC) is the most common malignant tumor of the digestive tract and its molecular mechanism is not clear. HOXD9 plays an important role in tumor progression as transcription factor. In the current study, we explored the role of HOXD9 in GC. Methods We predicted the expression and potential mechanism of HOXD9 in GC through an online database. The expression of HOXD9 was detected in GC and adjacent tissues, and then we analyzed the relationship between HOXD9 and the prognosis of patients with GC. In vitro, we investigated the effects of HOXD9 on malignant biological behaviors such as proliferation, migration, and invasion of the GC cell line MCG-803. In addition, we have initially studied the underlying mechanism by Western blot. Results High expression of HOXD9 in GC was predicted by online database prediction and implied poor prognosis. In the clinical sample, we confirmed the above predictions. In vitro, we found that knockdown of HOXD9 could effectively inhibit the proliferation, migration, and invasion of GC cells. In terms of mechanism, HOXD9 may activate the TGF-β/Smad signaling pathway. Conclusion HOXD9 promotes the malignant biological process of GC, which may be a potential therapeutic target for GC. © 2020 Xiong et al.Objective Glioma is the most common malignant brain tumor that has high aggressiveness. The aim of this study was to investigate the potential therapeutic targets for gliomas. Materials and Methods Real-time quantitative polymerase chain reaction (RT-qPCR) was employed to calculate the expression of miRNA and genes. The connection between the expression of miR-483 and patients’ overall survival rate was evaluated using Kaplan-Meier analysis. In addition, the underlying mechanism was detected using luciferase assay. Results The expression level of miR-483 was significantly decreased in glioma tissue samples and cell lines, compared to the adjacent tissues and normal cell lines. Downregulation of miR-483 or upregulation of SOX3 was associated with overall survival of glioma patients. Additionally, overexpression of miR-483 promotes cell invasion and migration and inhibits apoptosis. In addition, miR-483 directly targeted to SOX3, and the expression of miR-483 has a negative correlation with SOX3 in glioma tissues. SOX3 reversed partial functions of miR-483 on cell migration, invasion, and promoted cell apoptosis in glioma. Conclusion MiR-483 inhibited glioma cell migration, invasion, and promoted glioma cell apoptosis by targeting SOX3. MiR-483 maybe acted as a potential target for the treatment of glioma. © 2020 Lu et al.Introduction Because only a small portion of NSCLC (non-small-cell lung cancer) patients benefit from molecular targeted therapy or immunotherapy and do not develop therapeutic resistance, continued research on new targets is warranted. Serotonin has recently emerged as a growth factor for tumor cells, and its receptors may be potential therapeutic targets. The mechanism related to the behavior of the 5-HT7 receptor in NSCLC remains unknown. Methods Both gene expression analysis and immunohistochemical analysis were conducted to evaluate 5-HT7 receptor expression in NSCLC tissues. The correlation between 5-HT7 receptor expression and clinicopathological features was also examined. Cell proliferation was measured using a CCK8 (Cell Counting Kit-8) assay and colony formation, migration and invasion were evaluated by the Transwell assay. siRNA transfection and stimulation with the selective agonist LP211 were used to identify the involvement of molecules in proliferation, migration and invasion. Quantitative real-time chain reaction (qRT-PCR) and Western blotting were used to quantifiy mRNA and protein levels, respectively. Pathway inhibitors facilitated the exploration of possible signaling pathways regulated by the 5-HT7 receptor in migration and invasion. Results The 5-HT7 receptor was overexpressed in NSCLC tumor tissues compared with adjacent normal lung tissues. High 5-HT7 receptor expression levels were correlated with lymph node metastasis (P=0.007) and advanced TNM stage (P=0.000) in NSCLC patients. The 5-HT7 receptor positively regulated cell proliferation, migration and invasion in NSCLC cells. The stimulatory effect of the 5-HT7 receptor on A549 cell migration and invasion may occur through the P38 pathway. In H1299 cells, the 5-HT7 receptor might positively regulate Src to promote cell migration and invasion. Conclusion Our findings suggest that the 5-HT7 receptor, which mediates NSCLC progression, may be a potential therapeutic target. © 2020 Du et al.Background Hepatocellular carcinoma (HCC) is one of the most common malignancies worldwide and chemoresistance is the main obstacle for effective treatments of HCC. Accumulating studies indicated that long non-coding RNAs (lncRNAs) contribute to the chemoresistance of human carcinoma. However, the functional role of HANR in autophagy-mediated chemoresistance of HCC is unknown. Methods The expressions of HANR, miR-29b and ATG9A in tissues and cell lines were detected by real-time quantitative PCR (RT-qPCR). The expression of autophagy-related protein LC3-I and LC3-II was evaluated by Western blotting. The cell viability and apoptosis were examined by CCK-8 and flow cytometry, respectively. Bioinformatics analysis and luciferase activity assay were applied to determine the downstream target gene of HANR or miR-29b. Xenograft experiment was used to detect the effect of HANR on tumor growth. Results In the present study, we demonstrated that HANR was notably overexpressed in sorafenib-resistant HepG2 (HepG2/sora)l therapeutic strategies for HCC treatment. © 2020 Shi et al.Purpose The aim of this study was to explore the regulatory role and mechanism of long noncoding RNA LINC00152 in gastric cancer (GC) cells. Methods LINC00152 expression in GC tissues and cells was detected by reverse transcription-polymerase chain reaction (qRT-PCR). MKN45 and MGC-803 cells were selected and assigned into different groups after transfection with si-LINC00152, activated ERK/MAPK signaling pathway (SA), or negative control. Cell proliferation, apoptosis, cycle, migration and invasion were assessed by CCK-8, flow cytometry, Transwell assay and Scratch test, respectively. Western blot analysis was conducted to detect the expression of E-cadherin, N-cadherin and ERK/MAPK signaling pathway protein. Results Compared with the normal tissues, higher expression of LINC00152 was found in GC tissues and LINC00152 was remarkably correlative with clinical stage and lymphatic metastasis. LINC00152 expression in GC cells was higher than that in GES-1 cells. Compared with the NC group, the cell proliferation rate, cells in G2/M phase, migration and invasion abilities as well as the expression of N-cadherin and p-ERK-1/2 were significantly decreased, and the expression of E-cadherin, cells in G0/G1 phase and cell apoptosis rate were significantly increased in the si-LINC00152-1 group. ERK/MAPK signaling pathway activator SA could reverse the biological role of LINC00152 in GC cells. Conclusion These results demonstrated that the interference of LINC00152 expression may inhibit the invasion and migration of GC cells by inhibiting the ERK/MAPK signaling pathway. © 2020 Shi and Sun.Background Endometrial carcinoma (EC) is the primary cause of death associated with cancer globally. Thus, the possible molecular mechanism of EC needs further exploration. Up-frameshift protein 1 (UPF1) is an ATPase depending on RNA/DNA and RNA helicase depending on ATP. Long noncoding RNA (lncRNA) plasmacytoma variant translocation 1 (PVT1) was dysregulated in diverse diseases. Methods qRT-PCR and Western blot were applied to detect UPF1 and PVT1 in EC. CCK-8, colony formation, and Transwell assays were used to test the effects of UPF1/PVT1 on cell proliferation and migration. Cells were cultured with actinomycin D to observe mRNA stability, and RNA immunoprecipitation assay was applied to verified the relationship between UPF1 and PVT1. Glucose consumption and lactate generation were measured when cells were transfected with siRNA. Results Results demonstrated that the expression of UPF1 exhibited a remarkable decrement in EC tissues relative to that in non-tumor tissues. Subsequent functional experiments suggested that UPF1 decrement stimulated EC cells to grow and migrate. Moreover, UPF1 was discovered to be linked to PVT1 and had an inverse correlation with PVT1. Besides, PVT1 expression affected EC growth and migration, and PVT1 decrement alleviated the influence of UPF1 decrement on EC growth and migration and strengthened glycolysis in EC. Conclusion In this study, we found that UPF1 was down-regulated in EC tissues, and UPF1 might exert its role by regulating the expression of PVT1. © 2020 Xing et al.Background There is a large difference in postoperative survival in patients with non-metastatic colorectal cancer. We aimed to develop nomograms incorporating both hematological biomarkers and clinical characteristics to predict overall survival (OS) in patients with radical surgery for non-metastatic colorectal cancer. Methods A retrospective analysis was performed on date from 508 patients who underwent radical resection of colorectal cancer at the Affiliated Tumor Hospital of Guangxi Medical University from December 2011 to December 2015. Simple random sampling was performed by dividing these patients into a training set (n=355) and validation set(n=153), which yielded a 73 ratio in the sample sizes between these groups. Based on COX regression analysis of the results from the training cohort, a nomogram was developed to predict the three-year and five-year overall survival rate, and internal verification was also performed. The nomogram prediction accuracy and discriminating ability were evaluated by Harrell’s C-index (C-index), calibration curves and were compared with the colorectal cancer TNM staging system. Results We found that age, degree of differentiation, T stage, N stage, neurological invasion, neutrophils, monocytes, HGB, and LDH were independent risk factors for predicting OS in patients with colorectal cancer. In the training cohort, the C index was 0.796 (95% CI 0.761-0.831). In the validation cohort, the C index was 0.671 (95% CI 0.656-0.686).The nomogram showed a stronger predictive ability than did TNM staging. Decision curve analysis showed that the nomogram had value in terms of clinical application. Conclusion Our nomogram combined hematological biomarkers and clinical characteristics and was highly effective in predicting OS in patients with non-metastatic colorectal cancer. Hence, our nomogram may provide a reference tool for clinicians to guide individualized treatment and follow-ups for patients with colorectal cancer. © 2020 Long et al.