ABSTRACT
<p><b>OBJECTIVE</b>To explore the development of the study on Angiostrongylus cantonensis.</p><p><b>METHODS</b>A total of 930 papers were searched from the PubMed and Chinese Bio-medical Disc(CBM) database under the search terms of Angiostrongylus cantonensis and analyzed through publication time, journal and contents.</p><p><b>RESULTS</b>The number of papers published was found to increase annually, and two peaks of publication in national magazines occurred since 1996. Most papers were published in tropical medicine or professional journal of parasitology. The reports mostly documented cases and epidemiological investigations, and only a few investigated pathogenic mechanisms, drug treatment and other basic theory.</p><p><b>CONCLUSION</b>It is in the initial stage of the study on Angiostrongylus cantonensis and Angiostrongyliasis, and there are a vast space in diagnosis, pathogenic mechanism, therapy and prevalence of Angiostrongyliasis cantonensis.</p>
Subject(s)
Animals , Humans , Angiostrongylus cantonensis , Bibliometrics , China , Epidemiology , Data Collection , Strongylida Infections , EpidemiologyABSTRACT
OBJECTIVE@#To explore the effect of LRRC4, a glioma suppressive gene, on blocking U251 cells in G0/G1 by MAPK signaling pathway.@*METHODS@#LRRC4 was transfected into U251 cells, and at 24 hour of post-transfection, cells were split at a 1:3 dilution, challenged with 500 microg /mL G418 and formed a stable transfected clone pool. RT-PCR, Northern blot and Western blot were used to identify the stable transfectants. ERK, JNK and P38 expression changes were analyzed by Western blot. FACS analysis, Luciferase reporter gene assay and Western blot were used to detect the cell cycle and cyclin D1.@*RESULTS@#LRRC4 down-regulated the expression of phosphorylated ERK2 and up-regulated the expression of total protein JNK2 (a key molecule of MAPK signaling pathway) and phosphorylated c-Jun. LRRC4 decreased the expression of mutation P53, cyclin D1 activation and its expression. U251 cells were blocked in G0/G1 by LRRC4.@*CONCLUSION@#LRRC4 can decrease JNK2, up-regulate the phosphoralated c-Jun, down-regulate mutant P53 and cyclin D1, and therefore block U251 cells in G0/G1.
Subject(s)
Humans , Blotting, Northern , Blotting, Western , Cell Line, Tumor , Cyclin D1 , Metabolism , Flow Cytometry , G1 Phase , Genetics , Physiology , Glioma , Genetics , Metabolism , Pathology , Luciferases , Genetics , Metabolism , MAP Kinase Signaling System , Genetics , Physiology , Mitogen-Activated Protein Kinase Kinases , Metabolism , Nerve Tissue Proteins , Genetics , Metabolism , Physiology , RNA, Messenger , Genetics , Recombinant Fusion Proteins , Genetics , Metabolism , Resting Phase, Cell Cycle , Genetics , Physiology , Reverse Transcriptase Polymerase Chain Reaction , TransfectionABSTRACT
OBJECTIVE@#To examine the expression absence of LRRC4 gene in glioblastoma cell lines.@*METHODS@#RT-PCR and Northern blot were used to detect the expression of LRRC4 gene in 6 glioblastomas cells lines. Polymerase chain reaction and DNA sequencing were used to screen the LRRC4 gene mutation, while bioinformation assay was used to search for the reason of LRRC4 gene absence in U251 cell lines.@*RESULTS@#The expression of LRRC4 was absent in 6 malignant glioma cell lines (U251, U87, BT325, SF126, SF767 and M17), which were examined by Northern-blot and RT-PCR assay. All sequencing of PCR products from gDNA of SF126, SF767, and M17 cell lines contained the point mutation at the same position ( LRRC4 geneT977A) (3/5), which was a synonymous mutation. However, PCR products from gDNA of U251 and U87 cell lines (2/5) were not obtained. The expression absence of LRRC4 was ascribed to the loss of homozygosity of 7q32-ter in U251 cell lines.@*CONCLUSION@#The expression of LRRC4 gene is absent in glioblastoma cell lines, and it offers the important experiment proof for LRRC4 to act as a new candidate of brain tumor suppressor gene from glioma. The loss of homozygosity of 7q32-ter contributed to the expression absence of LRRC4 in U251 cell lines.