Bakertruelsen9645

The statistical analysis manifested that the highly expressed LINC01116 was positively correlated with the tumor-node-metastasis (TNM) stage (p=0.008), lymph node metastasis (p=0.005), and depth of invasion (p=0.007) of the GC patients. The patients with high expression of LINC01116 in the GC tissues had a shorter survival time than those with low expression (p=0.017). After interference in the expression of LINC01116, it was shown in CCK-8 assay and colony formation assay that the proliferative capacity of the cells was decreased. The results of flow cytometry indicated that the cell cycle was arrested at the G1/G0 phase, and the apoptosis rate was increased. CONCLUSIONS LINC01116 is highly expressed in GC tissues and cells, and highly expressed LINC01116 indicates poor prognosis of the patients, promotes the proliferation, and inhibits the apoptosis of GC cells.OBJECTIVE The application of intestinal microflora is involved in various cancers; however, researches reporting the potential of metabolites of intestinal microflora (MIM) on biological activities of colon cancer (CC) cells are unavailable. This study was designed to testify the functions of MIM on CC cells and its mechanism. MATERIALS AND METHODS qRT-PCR/Western blot were applied to test the expression levels of miR-192-5p and BMPR2 in human colonic epithelial cells and CC cells (HCT116, SW480). The effects of MIM, mimics-miR-192-5p or inhibitors-miR-192-5p on mRNA and protein expressions of miR-192-5p and BMPR2 were verified by qRT-PCR and Western blot. MTT assay for CC cell viability, flow cytometry for CC cells apoptosis rate, and cell scratch and cell chamber served for the analysis of invasion and migration ability of CC cells. The relationship between miR-192-5p and BMPR2 was validated employing Luciferase reporter gene assay. RESULTS Compared with human normal colonic epithelial cells, HCT116 and SW480 cells had lower expression of miR-192-5p and higher expression of BMPR2 (p less then 0.01). MIM and mimics-miR-192-5p could enhance cell apoptosis and suppress the migration and proliferation of CC cells. MIM were also found to up-regulate miR-192-5p and down-regulate the expression levels of BMPR2 and p-LIMK2 (p less then 0.01). Transfection of inhibitors-miR-192-5p reversed the inhibitory effect of MIM on CC cells. CONCLUSIONS MIM could up-regulate miR-192-5p to inhibit CC cell growth via down-regulating BMPR2 and inhibiting the activity of RhoA-ROCK-LIMK2 pathway.OBJECTIVE To investigate the expression of miR-130a in human colon cancer patients and its specific mechanism of regulating the biological function of colon cancer cells. PATIENTS AND METHODS Cancer tissues, paracancerous tissues, and serum samples of 40 colon cancer patients who underwent surgery in The Second Affiliated Hospital of Qiqihar Medical University from May 2018 to March 2019 were collected, and 40 healthy volunteers who received physical examination in The Second Affiliated Hospital of Qiqihar Medical University were collected. Real Time-quantitative Polymerase Chain Reaction (qRT-PCR) was used to detect the expression of miR-130a. Human colon cancer cell was divided into miR-130a mimic group, miR-130a inhibitor group, mimic NC (negative control), and inhibitor NC group. QRT-PCR was used to detect the expression of miR-130a, and MTT assay, colony formation assay, cell scratch assay, transwell assay were performed to detect cell viability, proliferation, migration, and invasion ability. RESULTS Coor colon cancer.OBJECTIVE The aim of this study was to explore the role of microRNA-802 (miRNA-802) in the progression of colorectal cancer (CRC) and the underlying mechanism. PATIENTS AND METHODS The relative expression levels of miRNA-802 and FOXE1 in 40 paired CRC tissues and adjacent normal tissues were detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). The correlation between miRNA-802 expression and the pathological indexes of CRC patients was assessed. Meanwhile, the prognostic potentials of miRNA-802 and FOXE1 in CRC patients were identified through the Kaplan-Meier method. After overexpression of miRNA-802, the changes in the proliferative, migratory, and invasive capacities of HT29 and HCT-8 cells were evaluated in vitro. The Dual-Luciferase Reporter Gene Assay was applied to investigate the binding relationship between miRNA-802 and FOXE1. Finally, the rescue experiments were carried out to uncover the role of the miRNA-802/FOXE1 axis in regulating the cellular behaviors of CRC. RESULTS MiRNA-ia negatively regulating FOXE1.OBJECTIVE Some studies have confirmed that long non-coding ribonucleic acids (lncRNAs) played a vital role in the pathophysiology of various diseases, especially in oncogenesis and progression of tumors. Dysexpressed lncRNAs regulate different cellular processes, including proliferation, invasion, and apoptosis. The aim of this study was to explore the clinical significance and function of lncRNA MIR4435-2HG in colorectal cancer. PATIENTS AND METHODS Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was performed to detect the expression of lncRNA MIR4435-2HG. The Kaplan-Meier method was used to evaluate the overall survival and disease-free survival of patients with colorectal cancer. AOA hemihydrochloride The cell proliferation was measured by Methyl thiazolyl tetrazolium (MTT) assay. The cell apoptotic rate was measured via flow cytometry method. RESULTS LncRNA MIR4435-2HG is a novel cancer-related lncRNA that was recently found to exhibit high expression in colorectal cancer. The dysregulation of lncRNA miR4435-2HG was significantly related to the tumor size (p less then 0.001), lymph node metastasis (p less then 0.001), and tumor node metastasis (TNM) staging (p=0.022). The patients with higher expression of lncRNA miR4435-2HG showed worse prognosis than those with low expression of lncRNA miR4435-2HG group. Besides, the downregulated lncRNA miR4435-2HG expression could repress cell proliferation and enhance cell apoptosis. CONCLUSIONS LncRNA MIR4435-2HG functions as an oncogene that promotes colorectal cancer progression, and likely represents a biomarker or therapeutic target of colorectal cancer.