Objective:To investigate the role of O-GlcNAcylation in the regulation of the stability of receptor for activated C kinase 1(Rack1)during SHH-type medulloblastoma(SHH-MB)initiation.Methods:SHH-MB tumors and adjacent tissues were selected from the clinical tu-mor specimen library of the Department of Pathology at The General Hospital of Western Theater Command.Rack1 expression and O-GlcNAcylation(O-GlcNAc)levels in these tumor tissues were analyzed.The human medulloblastoma cell line Daoy was treated with a glyc-osyltransferase(OGT)inhibitor(OSMI-1)and adeglycosyltransferase(OGA)inhibitor(TM-G),and their impact on tumor cell proliferation was assessed using a Cell Counting Kit-8(CCK-8)and immunofluorescence staining.The O-GlcNAc enzyme labeling system co-immunoprecipita-tion(Co-IP)and Western blot were used to correlate Rack1 protein levels with O-GlcNAc levels.The impact of O-GlcNAcon Rack1 stability was confirmed using cycloheximide(CHX)and ubiquitination modification experiments.In a medulloblastoma mouse model with Rack1 knockdown,tumor cell proliferation was detected using a Cell Counting Kit-8(CCK-8),immunofluorescence staining,and a scratch assay.Xenograft tumors were transplanted into immunodeficient mice and SHH signaling was detected by Western blot in the obtained tissue samples(sh-NC and sh-Rack1)to verify the role of Rack1 protein in SHH-MB.Results:Rack1 and O-GlcNAcylation levels were significantly in-creased in SHH-MB tumor samples,and a negative correlation was observed between Rack1 levels and patient survival rates.Treatment of Daoy cells with OGT and TM-G revealed that O-GlcNAc significantly promotes Daoy cell proliferation,while inhibiting O-GlcNAc impedes tu-mor cell proliferation.Molecular experiments have confirmed that O-GlcNAc modification of Rack1 protein can regulate tumor cell stability,thereby promoting tumor cell proliferation.When Rack1 expression was knocked down in Daoy cells,cell proliferation was significantly re-duced relative to control cells.Accordingly,proliferation was significantly inhibited in tumor tissues with Rack1 protein knockdown in mouse models,suggesting that Rack1 can participate in the initiation of SHH-MB by regulating SHH signaling.Conclusions:O-GlcNAcylation particip-ates in SHH-MB initiation by regulating Rack1 stability.

Objective:To investigate the role of O-GlcNAcylation in the regulation of the stability of receptor for activated C kinase 1(Rack1)during SHH-type medulloblastoma(SHH-MB)initiation.Methods:SHH-MB tumors and adjacent tissues were selected from the clinical tu-mor specimen library of the Department of Pathology at The General Hospital of Western Theater Command.Rack1 expression and O-GlcNAcylation(O-GlcNAc)levels in these tumor tissues were analyzed.The human medulloblastoma cell line Daoy was treated with a glyc-osyltransferase(OGT)inhibitor(OSMI-1)and adeglycosyltransferase(OGA)inhibitor(TM-G),and their impact on tumor cell proliferation was assessed using a Cell Counting Kit-8(CCK-8)and immunofluorescence staining.The O-GlcNAc enzyme labeling system co-immunoprecipita-tion(Co-IP)and Western blot were used to correlate Rack1 protein levels with O-GlcNAc levels.The impact of O-GlcNAcon Rack1 stability was confirmed using cycloheximide(CHX)and ubiquitination modification experiments.In a medulloblastoma mouse model with Rack1 knockdown,tumor cell proliferation was detected using a Cell Counting Kit-8(CCK-8),immunofluorescence staining,and a scratch assay.Xenograft tumors were transplanted into immunodeficient mice and SHH signaling was detected by Western blot in the obtained tissue samples(sh-NC and sh-Rack1)to verify the role of Rack1 protein in SHH-MB.Results:Rack1 and O-GlcNAcylation levels were significantly in-creased in SHH-MB tumor samples,and a negative correlation was observed between Rack1 levels and patient survival rates.Treatment of Daoy cells with OGT and TM-G revealed that O-GlcNAc significantly promotes Daoy cell proliferation,while inhibiting O-GlcNAc impedes tu-mor cell proliferation.Molecular experiments have confirmed that O-GlcNAc modification of Rack1 protein can regulate tumor cell stability,thereby promoting tumor cell proliferation.When Rack1 expression was knocked down in Daoy cells,cell proliferation was significantly re-duced relative to control cells.Accordingly,proliferation was significantly inhibited in tumor tissues with Rack1 protein knockdown in mouse models,suggesting that Rack1 can participate in the initiation of SHH-MB by regulating SHH signaling.Conclusions:O-GlcNAcylation particip-ates in SHH-MB initiation by regulating Rack1 stability.

OBJECTIVETo explore the relationship between the structure and function at molecular level and the routes of transmission of Xinjiang hemorrhagic fever (XHF) virus.

METHODSS genes of five XHF virus strains were cloned, sequenced and compared with that of other Crimean-Congo hemorrhagic fever virus strains.

RESULTSIt was found that S genes of the five viruses had 1,672 nuclei tides, while ORF of them including 1,449 nuclei tides and coded with a protein of 482 amino acid. The nucleotides homology of Chinese isolates (93.0%-99.5%) was obviously higher than that of any other S genes strains identified in other countries'. Phylogenetic tree showed that all Chinese isolates clustered into one branch and could be further divided into another three groups.

CONCLUSIONThe sequential difference of S genes was not totally related to the host, areas and time of the viruses isolated.

Genes, Bacterial ; Genetic Variation ; Hemorrhagic Fever Virus, Crimean-Congo ; classification ; genetics ; Phylogeny