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Affect associated with COVID-19 lockdown steps in institutional delivery, neonatal acceptance and also prematurity: an expression from Lagos, Africa.
OBJECTIVE Colorectal cancer is a common malignant tumor of the digestive tract, and its incidence is closely related to lifestyle inheritance and colorectal adenoma. Circular RNA (circRNA) has been proved to participate in the progression of colorectal cancer cells. Our study aimed to investigate the function and the underlying mechanism of circRNA circDENND4C in colorectal cancer cells. PATIENTS AND METHODS The expression of circDENND4C, glucose transporter 1 (GLUT1), and miR-760 was detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Western blot was used to measure the protein levels of GLUT1, the proliferation-related protein (Cyclin D1) and matrix metallopeptidase 9 (MMP-9). Cell Counting Kit-8 (CCK-8) assay and transwell assay were performed to evaluate cell proliferation and migration. The glucose uptake and lactate production were detected by the corresponding kits. The targets between circDENND4C and miR-760 and miR-760 and GLUT1 were predicted by starBase 3.0 and TargetScan, and then confirmed by Dual-Luciferase reporter assay. Animal experiment revealed the effect of circDENND4C on colorectal cancer cells in vivo. RESULTS The expression of circDENND4C and GLUT1 was upregulated in colorectal cancer tissues and cells. Functionally, the knockdown of circDENND4C suppressed proliferation, migration, and glycolysis of colorectal cancer cells. Similarly, silence of GLUT1 also inhibited cell proliferation, migration, and glycolysis. Notably, the overexpression of GLUT1 reversed the functional effects of circDENND4C knockdown on colorectal cancer cells. More importantly, miR-760 acted as a direct target of circDENND4C, and miR-760 could bind to GLUT1, and circDENND4C regulated GLUT1 by sponging miR-760. Finally, circDENND4C knockdown decreased the growth of colorectal cancer cells in vivo. CONCLUSIONS CircRNA circDENND4C accelerated proliferation, migration, and glycolysis of colorectal cancer cells through regulating GLUT1 by sponging miR-760.OBJECTIVE We sought to uncover the potential role of long non-coding RNA (lncRNA) ADPGK-AS1 in colorectal cancer (CRC). PATIENTS AND METHODS ADPGK-AS1 levels in 58 pairs of CRC tissues and paracancerous tissues and 30 normal colorectal tissues were determined. The in vitro level of ADPGK-AS1 in CRC cell lines was tested as well. The regulatory effects of ADPGK-AS1 on the proliferative, migratory, and invasive properties of HCT116 and SW480 cells were assessed. Using a Dual-Luciferase reporter gene assay, the interaction among ADPGK-AS1/miR-525/FUT1 was identified. Finally, potential influences of the regulatory loop ADPGK-AS1/miR-525/FUT1 on the phenotypes of CRC cells were explored. RESULTS ADPGK-AS1 was upregulated in CRC tissues and cells. Knockdown of ADPGK-AS1 attenuated the proliferative, migratory, and invasive abilities of CRC cells. Meanwhile, miR-525 was confirmed to be the target of ADPGK-AS1 and FUT1 was the downstream gene binding miR-525. The regulatory loop ADPGK-AS1/miR-525/FUT1 was found to aggravate the malignant progression of CRC. CONCLUSIONS ADPGK-AS1 is upregulated in CRC. The regulatory loop ADPGK-AS1/miR-525/FUT1 exacerbates the progression of CRC by promoting the proliferation, migration, and invasion of tumor cells.OBJECTIVE Long noncoding RNA sex determination region of Y chromosome (SRY)-related HMG-box (SOX) is involved in the development of various cancers. However, the molecular mechanism of SOXOT, an overlapping transcript of SOX, in pancreatic cancer (PC) is still undefined. We aimed to explore the epigenetic function of SOX2OT and its downstream factors in advanced PC. PATIENTS AND METHODS The levels of SOX2OT, miRNA, and DEK proto-oncogene (DEK) in pancreatic cancer tissues and cell lines were evaluated by quantitative polymerase chain reaction (qPCR). The log-rank test was applied to evaluate the role of high SOX2OT levels in shortening the overall survival of pancreatic cancer patients. CC-92480 ic50 The Chi-squared test was made to assess the relation between SOX2OT expression and clinicopathological features of PC patients. Colony assay tested the cell proliferation of PC cells with SOX2OT knockdown. Flow cytometry and Western blotting were used to determine the stemness of tumor cells in vitro. The underlying regulatory mechanism between SOX2OT and miR-200a/141 was predicted by bioinformatics and verified by RNA transfection, qPCR, and Western blotting. Mice xenograft models were applied to determine the promoting effects of SOX2OT on PC in vivo. RESULTS The expression of SOX2OT in PC tissues and cell lines is strongly elevated. High levels of SOX2OT expression are more likely to present in patients with advanced TNM stage, positive CD44, and poor overall survival. SOX2OT overexpression promotes proliferation and stemness maintaining of PC cells in vitro and boosts tumor growth in vivo. Furthermore, SOX2OT upregulates DEK expression by binding to miR-200a/141 as a competing endogenous RNA. CONCLUSIONS DEK induced by SOXOT- miR-200a/141 axis may markedly promote stem cell property of PC, resulting in an advanced stage and inferior survival. These findings suggest the SOX2OT-DEK axis as a novel therapeutic target in PC.OBJECTIVE This study aimed to explore the expression and clinical significance of LINC01197 in serum of patients with pancreatic cancer (PC). PATIENTS AND METHODS Fifty PC patients (patient group) treated in our hospital from March 2012 to April 2014 were collected, and another 50 normal people (normal group) were collected for physical examination. The LINC01197 expression in serum of the two groups was detected by qRT-PCR method, and the CA 19.9 expression in serum was detected by Roche automatic biochemistry. The expression and diagnostic value of CA 19.9 and LINC01197 in PC were analyzed, and the relationship between LINC01197 and prognosis of PC patients was observed. RESULTS The CA 19.9 expression in the patient group was significantly higher than that in the normal group (p less then 0.001). Their area under the curve was 0.791 and 0.944 respectively. The incidence of phases III+IV, lymphatic invasion, and distant metastasis in patients with low expression of LINC01197 is significantly higher than that in those with high expression, and has higher diagnostic value.
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