ABSTRACT
OBJECTIVE: To investigate the expression of microRNA-622(miR-622)in epithelial ovarian cancer,andanalyze its influence on tumor cell migration and invasion.METHODS:Epithelial ovarian cancer(n=125),benignepithelial ovarian tumors(n=45),and normal ovarian tissues(n=25)were obtained from January 2003 to December 2016 at Dongguan People's Hospital of Southern Medical University.The expression of miR-622 was determined by real-timePCR.The miR-622 mimics were transiently transfected into human ovarian cancer cells,and their influence on cellmigration and invasion was analyzed by Transwell assay.RESULTS:Higher miR-622 expression was found in epithelialovarian cancer tissues than in benign epithelial ovarian tumors and normal ovarian tissues(P<0.05).Expression of miR-622 was correlated with FIGO stage and lymphatic metastasis(P<0.05).Up-regulation of miR-622 promoted theinvasion and migration of SKOV3 cells in vitro.CONCLUSION:The expression level of miR-622 is increased in tumourtissues,which indicates that miR-622 might be involved in the progression of epithelial ovarian cancer by promotingcancer cell migration and invasion.
ABSTRACT
[Objective] To investigate the expression of microRNA-200c (miR-200c) in colorectal carcinomas (CRC),and analyze its role on tumor cell migration and invasion.[Methods] The expression levels of miR-200c in CRC tissues and adjacent normal mucosa were assessed by real-time quantitative RT-PCR (qRT-PCR).miR-200c mimics were transiently transfected into human colorectal cancer cells,and their roles on cell migration and invasion were analyzed by Transwell assay.Cell proliferation was measured using the Cell Counting kit-8.The expression levels of epithelial and mesenchymal markers as well as related transcription factor ZEB1 were detected by Western blotting.[Results] Lower miR-200c expression was found in primary CRC tissues with lymph node metastasis compared to those without lymph node metastasis and adjacent normal mucosa.Transfection of miR-200c mimics suppressed proliferation,and reduced invasion and migration in SW620 cells.Furthermore,up-regulation of miR-200c inhibited ZEB1,and resulted in increased E-cadherin and reduced Vimentin gene expression.[Conclusion] miR-200c was associated with invasive and metastatic behavior of CRC.These effects may be mediated through regulation of epithelial-mesenchymal transition.
ABSTRACT
<p><b>OBJECTIVE</b>To investigate the inhibition effect of leukemic bone marrow stromal cells (BMSCs) on daunorubicin (DNR) induced apoptosis of human Jurkat cell line, and analyze the differentially expressed genes between Jurkat cells cocultured with leukemic BMSCs or without.</p><p><b>METHODS</b>Suppression subtractive hybridization (SSH) was employed to establish subtracted cDNA library of differentially expressed genes in Jurkat cells cocultured with leukemic BMSCs and DNR. The cDNA fragments were sequenced and analyzed.</p><p><b>RESULTS</b>The differentially expressed gene cDNA library was successfully developed. Primary screening was done by reverse Northern hybridization. Thirty up-regulated and 22 down-regulated cDNA fragments were isolated and sequenced. Analysis and comparison were performed in GenBank using BLAST. These genes are related to cell cycle regulation, cell apoptosis and energy metabolism.</p><p><b>CONCLUSION</b>Leukemic BMSCs influence gene expression of Jurkat cells. The resulting differentially expressed genes might be associated with the protection of leukemic cells by BMSCs from injury.</p>
Subject(s)
Humans , Apoptosis , Bone Marrow Cells , Metabolism , Pathology , Cells, Cultured , Coculture Techniques , Daunorubicin , Pharmacology , Gene Expression Profiling , Gene Expression Regulation, Leukemic , Gene Library , Jurkat Cells , Stromal Cells , Metabolism , PathologyABSTRACT
The bone marrow microenvironment composed of bone marrow cell, their secreted cytokines and extra-cellular medium (ECM), plays an important role in the process of hematopoiesis, hematonosis, apoptosis of malignant blood cells. In this review, the mechanisms for the protection of the leukemiic cells from the drug-induced apoptosis by bone marrow stromal cells and the related progress were summarized.