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  • '); var ntfc_preview = ''; $.post('/api/v1/get_notifications', function(r) { var ntfc_read_pending = 0; var ntfc_pending = 0; $.each(r.notifications.pending, function(index, ntfc_object) { ntfc_read_pending++; ntfc_pending++; if (ntfc_read_pending
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  • '); $('.notification-count').hide(); } data = {'nid' : '', 'ntid' : 1}; $.post('/api/v1/notification_action', data, function(r) { if (r.request == 'OK') { $('.notification-count').hide(); } }); }, "json"); }); $('.search-save-box').on({ click : function(e) { e.preventDefault(); var search_attr = $(this).attr('rel').split(','); var p = search_attr[1]; var tf = search_attr[0]; window.location = '/search?tf='+tf+'&jc='+jc+'&keywords='+$(this).html()+'&s='+$('#sort_order').val()+'&p='+p; } }, '.search-name'); $( "#keywords_main, #keywords_mobile" ).focus(function(e) { show_saved_searches(e, $(this)); }); $(window).resize(function () { if ($('.search-save-box').is(':visible')) { if ($('#keywords_main').is(':visible')) var left_search_save = $('#keywords_main').offset().left; if ($('#keywords_mobile').is(':visible')) var left_search_save = $('#keywords_mobile').offset().left; $('.search-save-box').css('left',left_search_save); } }); $('.search-save-box').on({ click : function(e) { e.preventDefault(); delete_saved_search($(this)); } }, '.search-name-close'); $('.search-save-box, #keywords_main, #keywords_mobile').click(function(e) { e.stopPropagation(); }); $(document).click(function(e) { $('.search-save-box').hide(); }); $( "#keywords_main, #keywords_mobile" ).autocomplete({ source: function( request, response ) { // data contains the JSON object textStatus contains the status: success, error, etc $.post('/api/v1/searches', {'key' : request.term}, function(data, textStatus) { response(data); }, "json") }, select: function (event, ui) { var reportname = ui.item.value; var thelinks = '/search?tf='+$('#time_frame').val()+'&jc='+jc+'&keywords='+reportname+'&s='+$('#sort_order').val()+'&p='+$('#people_cluster').val(); } }); $('.search-go').click(function(e) { e.preventDefault(); window.location = get_search_url(); }); $('.logout').click(function(e) { e.preventDefault(); }); $('.header_keywords, .home_page_keywords').on('keydown', function(e) { if (e.keyCode == 13) { window.location = get_search_url(); } $('.search-save-box').hide(); }); $('.seemore').click(function(e){ e.stopImmediatePropagation(); }); });
    Sep 09, 2015
    Iranian Journal Of Basic Medical Sciences
    OBJECTIVES: Eukaryotic translation initiation factor 4E (eIF4E) is overexpressed in cervical cancer (CC). However, the molecular mechanisms are unclear. This study aimed to investigate the molecular mechanism of eIF4E gene overexpression in CC. MATERIALS AND METHODS: The human papillomavirus (HPV) type 18 E7 and eIF4E mRNAs were measured following knock down or overexpression of E7 gene by RT-PCR and real-time PCR. Cell counting kit-8 assay was used to determine the cell proliferation. Flow cytometry was used to analyze the cell cycle and apoptosis. Transwell system was employed to determine the cell migration. RESULTS: Overexpression of E7 gene increased eIF4E mRNA level by 24.3% (P<0.01) in HPV negative C33A cells. Knock down of E7 decreased markedly eIF4E mRNA by 73% (P<0.01) in HPV18 positive HeLa cells. Under the state of high expression of E7, 1) up-regulation of eIF4E drastically promoted the cell proliferation, cell cycle and cell migration, and inhibited the cell apoptosis. 2) down-regulation of eIF4E significantly inhibited the cell proliferation, cell cycle and the ability of cell migration, and also promoted the apoptosis of cervical cancer cells. CONCLUSION: HPV E7 induced eIF4E gene over transcription which might be a new marker for CC. The finding broadens the understanding of the CC carcinogenesis.
      
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