Funchcantu1789

found remarkably increased in both PCa tissues and cell lines, which was remarkably associated with pathological stage and incidence of distant metastasis of PCa patients. In addition, UNC5B-AS1 was able to accelerate the malignant progression of PCa by modulating caspase-9 expression.OBJECTIVE The importance of circular RNAs in malignant tumors has attracted a lot of attention. Circular PSMC3 (CircPSMC3) is identified as a tumor suppressor in gastric cancer. The role of circPSMC3 in prostate cancer (PCa) remains unclear. Our study aims to uncover whether and how circPSMC3 functions in PCa development. PATIENTS AND METHODS Real Time-quantitative Polymerase Chain Reaction (RT-qPCR) was utilized to determine the level of circPSMC3 in PCa tissues and cell lines. The relation between circPSMC3 expression and patients' prognosis was analyzed as well. CircPSMC3 lentivirus was constructed and transfected into PCa cells. Cell migration and invasion abilities were detected through wound healing assay, transwell assay, and Matrigel assay, respectively. Western blot assay was performed to detect the protein level of DGCR8. RESULTS CircPSMC3 was lowly expressed in PCa tissues compared with adjacent normal tissues. Low expression of circPSMC3 was significantly downregulated in PCa cell lines as well. The migration and invasion abilities of PCa cells were significantly inhibited after circPSMC3 was overexpressed in vitro. Furthermore, DGCR8 expression increased remarkably via the overexpression of circPSMC3. CONCLUSIONS CircPSMC3 could suppress PCa cell migration and invasion by upregulating DGCR8.OBJECTIVE Ovarian cancer (OC) is still the third leading cause of death in reproductive system malignancies. In OC, the biological function of microRNA-202-5p (miR-202-5p) is unknown. Our current research mainly focuses on miR-202-5p in the OC progression. PATIENTS AND METHODS MiR-202-5p was determined to be down-regulated in OC by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Cell counting kit-8 (CCK-8) assay and colony formation assay were recruited to access the ability of miR-202-5p on cell proliferation. Cell migration and invasion were determined by transwell assay and Matrigel assay. Dual-Luciferase reporter assay was recruited, and it validated that HOXB2 was a downstream target of miR-202-5p. Epithelial-mesenchymal transition (EMT) hallmark genes and HOXB2 expression level were examined by Western blotting. RESULTS MiR-202-5p was down-expressed in OC. Receiver operating characteristic (ROC) curve indicated that miR-202-5p was positively related to HOXB2. Staurosporine MiR-202-5p over-expression led to a higher 5-year survival rate. Up-regulated miR-202-5p inhibited cell proliferation and metastasis in vitro. HOXB2 was a downstream target of miR-202-5p. CONCLUSIONS We verified that miR-202-5p suppressed cell proliferation, migration, and invasion in OC via regulating HOXB2. Our findings provide new insights into the underlying mechanism of OC progression and may be useful in finding biomarkers and therapeutic targets of OC.OBJECTIVE The aim of this study was to uncover the role of lncRNA MIF-AS1 in influencing the biological phenotypes of ovarian cancer (OC) and the underlying mechanism. PATIENTS AND METHODS OC tissues and adjacent normal tissues were collected from 50 OC patients. The expression level of lncRNA MIF-AS1 in OC tissues and cells was determined by quantitative Real-Time Polymerase Chain Reaction (qRT-PCR). The prognostic potential of MIF-AS1 in OC patients was assessed by the Kaplan-Meier method. Subsequently, the regulatory effects of MIF-AS1 on proliferative, migratory, and invasive abilities of ES-2 and HO-8910 cells were evaluated by a series of functional experiments. Dual-Luciferase reporter gene assay, qRT-PCR, and Western blot were further conducted to verify the interaction in the regulatory loop MIF-AS1/miRNA-31-5p/PLCB1. RESULTS MIF-AS1 was significantly upregulated in OC tissues and cell lines (p less then 0.05). Higher level of MIF-AS1 predicted significantly worse prognosis of OC patients (p less then 0.05). The knockdown of MIF-AS1 markedly attenuated the proliferative, migratory, and invasive abilities of ES-2 and HO-8910 cells (p less then 0.05). Dual-Luciferase reporter gene assay verified that MIF-AS1 competed with PLCB1 to bind miRNA-31-5p. In addition, MIF-AS1 negatively regulated miRNA-31-5p expression cells, and miRNA-31-5p negatively regulated PLCB1 expression in OC. CONCLUSIONS MIF-AS1 was significantly upregulated in OC, which accelerated the proliferative, migratory, and invasive abilities of OC cells. Furthermore, the regulatory loop MIF-AS1/miRNA-31-5p/PLCB1 could be utilized as a therapeutic target for OC.OBJECTIVE MicroRNAs (miRNAs) are endogenous, non-coding small RNAs involving in pathological regulation. Previous studies have shown that microRNA-29c-3p is a tumor-suppressor gene. However, the role of microRNA-29c-3p in osteosarcoma (OS) has not been reported. This study aims to investigate the potential influence of microRNA-29c-3p on the progression of OS. PATIENTS AND METHODS Quantitative Real-Time Polymerase Chain Reaction (qRT-PCR) was applied to examine microRNA-29c-3p levels in 40 matched pairs of OS tumor tissues and adjacent ones. The correlation between microRNA-29c-3p expression and clinical indicators in OS patient was analyzed. At the same time, qRT-PCR was used to detect microRNA-29c-3p level in OS cell lines. In addition, microRNA-29c-3p knockdown and the overexpression models were constructed in OS cell lines. The effects of microRNA-29c-3p on the biological functions of OS cells were analyzed via cell counting kit-8 (CCK-8) and transwell assays. Finally, the potential mechanism underlying mth distant metastasis and poor prognosis. MicroRNA-29c-3p might inhibit the malignant progression of OS by modulating PIK3R3 expression.OBJECTIVE Osteosarcoma (OS) is a frequent bone malignancy. Long non-coding RNA myocardial infarction associated transcript (MIAT) has been reported to be involved in the development of human cancers, including OS. However, the mechanism underlying MIAT in OS progression remains largely unclear. PATIENTS AND METHODS The expression levels of MIAT and sineoculis homeobox homolog 1 (SIX1) in OS tissues and cells were detected by quantitative real-time polymerase chain reaction and Western blot. Cell viability, apoptosis, migration and invasion of OS cells were determined by MTT, flow cytometry and trans-well assays, respectively. The target interaction among MIAT, miR-141-3p and SIX1 was analyzed by bioinformatics analysis and luciferase reporter assay. Phosphatidylinositide 3-kinases (PI3K)/protein kinase B (AKT) pathway was evaluated by Western blot. RESULTS MIAT and SIX1 expression levels were enhanced in OS tissues and cells. Knockdown of MIAT or SIX1 repressed cell viability, migration and invasion but promoted apoptosis in OS cells. Moreover, overexpression of SIX1 reversed the inhibitive role of MIAT silence in OS progression. Furthermore, MIAT could increase SIX1 expression by competitively sponging miR-141-3p. Besides, inhibition of MIAT blocked PI3K/AKT pathway by decreasing SIX1 in OS cells. CONCLUSIONS MIAT silence suppresses OS progression through inactivating PI3K/AKT signaling by sponging miR-141-3p to regulate SIX1, indicating a novel target for the treatment of OS.OBJECTIVE Many findings have demonstrated long noncoding RNAs (lncRNAs) as crucial regulatory molecules in the progression of osteosarcoma. The aim of this study was to explore the roles and mechanisms of LncRNA LINC00689 (LINC00689) in osteosarcoma. PATIENTS AND METHODS Differential levels of LINC00689 and miR-655 in osteosarcoma samples and cell lines were analyzed by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). The associations between LINC00689 expression and prognostic significance of osteosarcoma patients were analyzed using a series of statistical assays. Loss-of-function and gain-of-function assays were performed to investigate the role of LINC00689 in proliferation and metastasis in vitro. Bioinformatic assays, Luciferase report assays, and rescue assays were applied to illustrate the ceRNA mechanism network of LINC00689/miR-655/SOX18. RESULTS We found that LINC00689 expression was distinctly upregulated in osteosarcoma specimens and cell lines. MiR-655 displayed a trend of remarkably decreased expression in osteosarcoma tissues. In addition, we showed that LINC00689 could specifically interact with the promoter of SP1 and activate LINC00689 transcription. Further clinical studies indicated that higher levels of LINC00689 were associated with advanced clinical stage, positively distant metastasis, and unfavorable clinical outcome. Functional studies revealed that the knockdown of LINC00689 suppressed the proliferation, migration, and invasion of osteosarcoma cells, and promoted apoptosis. Final mechanistic investigations confirmed that upregulation of LINC00689 competitively bound to miR-655 that prevented SOX18 from miRNA-mediated degradation, thus facilitating osteosarcoma progression. CONCLUSIONS All our findings suggested that SP1-induced upregulation of LINC00689 promoted osteosarcoma progression by regulating miR-655/ SOX18 axis, which provided a novel insight for osteosarcoma tumorigenesis.OBJECTIVE To assess the value of the simultaneous application of ultrasound and sialendoscopy (US+SE) in several salivary gland diseases not caused either by sialolithiasis or by tumours. PATIENTS AND METHODS US+SE are routinely used in patients with inflammatory, obstructive, and other non-tumorous major salivary gland diseases. In patients in whom US and SE as single investigation tools were not conclusive or not useful in the management of several non-sialolithiasis-related conditions (stenoses, ductal anomalies, ductal trauma, space-occupying paraductal lesions), both methods were used simultaneously for diagnosis and treatment. RESULTS US+SE were used simultaneously in 44 patients for 56 indications. Stenosis was managed in 36 cases (81.8%) and in thirty-eight of the indications (67.9%) with simultaneous US+SE. The successful opening was achieved in 23 (63.9%), conservative and/or ablative treatment was indicated in 13 (36.1%), and further imaging was indicated in two (5.5%) of these cases. Post-traumatic or postinfectious complications were managed in 12 (27.3%) of all cases, and isolated ductal anomalies and paraductal space-occupying lesions were assessed in three cases (8.3%) each. In all instances, simultaneous US+SE clearly improved the management in diagnosis and/or therapy. CONCLUSIONS  Simultaneous application of US+SE provided additional information that proved to be valuable for diagnosis, planning, and treatment in several non-sialolithiasis-related conditions such as stenoses, ductal anomalies, ductal trauma, and space-occupying paraductal lesions.OBJECTIVE To explore the relationship between micro ribonucleic acid (miR)-375 in regulating the N-Myc downstream-regulated gene 2 (Ndrg2)/interleukin-6 (IL-6)/signal transducer and activator of transcription 3 (STAT3) signaling pathway and diabetic retinopathy (DR) in rats. MATERIALS AND METHODS Thirty Sprague- Dawley rats were randomly divided into Control group (n=10), Model group (n=10), and miR-375 inhibitor group [miR-375 small interfering RNA (siRNA) group, n=10]. The rats in Model group were injected with streptozotocin (STZ) via the tail vein to prepare into rat models of diabetes. The body weight, fasting blood glucose, and retinal barrier permeability of rats in each group were detected. The levels of malondialdehyde (MDA) and superoxide dismutase (SOD) in rat serum were measured using kits. Terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate-biotin nick end labeling (TUNEL) assay was performed to determine the apoptosis of optic ganglion cells in rat retinal tissues. Additionally, the messenger RNA (mRNA) and protein levels of Ndrg2, IL-6 and STAT3 in rat retinal tissues were detected via reverse transcription-polymerase chain reaction (RT-PCR) and Western blotting, respectively.