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Keywords {🔍}

igfbp, mira, expression, pubmed, cancer, article, cell, google, scholar, cells, fig, gastric, cas, analysis, survival, protein, central, mrna, tcga, cohort, samples, growth, primary, mkn, control, lines, hong, gene, binding, kong, additional, compared, type, role, assays, experiments, poor, file, group, site, potential, upregulated, proliferation, showed, tumor, table, overexpression, molecular, kang, mirna,

Topics {✒️}

modulating pi3k/akt/survivin pathway igf2 mrna-binding proteins c-terminal messenger ribonucleoprotein 3rd cancer-related death di martino mt pi3k/akt/survivin pathway [50 article download pdf distinct rna-binding domains complex cancer genomics rna-binding protein insulin low-expression mir-34a group c-terminal kh domains anti-mouse igg-hrp anti-rabbit igg-hrp mir-34a blocks osteoporosis rna-binding protein g0/g1 phase cells g0/g1-phase cells triple-negative breast cancer synthetic mir-34a mimics mir-34a mimics delivered mir-34a recognition site state key laboratory mir-34a showed uniformly tumor-suppressive mir-34a histone-deacetylase inhibitor trichostatin cancer-related death mirna precursor mir-34a mir-34a expression showed ncbi/geo/gse62254 related subjects small-cell lung cancer mir-34a overexpression resulted mir-34a-dependent overexpression promotes cancer proliferation ncbi/geo/gse63089 mir-34a transfectants compared cell cycle regulators ectopic mir-34a expression called intestinal-type carcinoma promote cell growth g0/g1 phase full access promote tumor growth multiple putative targets mir-34a transfected cells dysregulated related mirnas mir-34a overexpression decreased privacy choices/manage cookies cell invasion ability

Questions {❓}

• Insulin-like growth factor 2 mRNA-binding proteins (IGF2BPs): post-transcriptional drivers of cancer progression?
• Mir-34: a new weapon against cancer?

Schema {🗺️}

WebPage:
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         headline:IGF2BP3 functions as a potential oncogene and is a crucial target of miR-34a in gastric carcinogenesis
         description:Gastric cancer (GC) is one of the frequent causes of cancer-related death in eastern Asian population. IGF2BP2 lists in the top rank up-regulated genes in GC, but its functional role is unclear. The expression of IGF2BP3 in GC cell lines and primary samples was examined by qRT-PCR and Western blot. The biological role of IGF2BP3 was revealed by a series of functional in vitro studies. Its regulation by microRNAs (miRNAs) was predicted by TargetScan and confirmed by luciferase assays and rescue experiments. IGF2BP3 ranked the No.1 of the up-regulated genes by expression microarray analysis in GC cell lines. The expression level of IGF2BP3 was observed in GC tissues comparing with non-tumorous gastric epitheliums. The up-regulated IGF2BP3 expression was associated with poor disease specific survival. IGF2BP3 knockdown significantly inhibited cell proliferation and invasion. Apart from copy number gain, IGF2BP3 has been confirmed to be negatively regulated by tumor-suppressive miRNA, namely miR-34a. The expression of miR-34a showed negative correlation with IGF2BP3 mRNA expression in primary GC samples and more importantly, re-overexpression of IGF2BP3 rescued the inhibitory effect of miR-34a. We compressively revealed the oncogenic role of IGF2BP3 in gastric tumorigenesis and confirmed its activation is partly due to the silence of miR-34a. Our findings identified useful prognostic biomarker and provided clinical translational potential.
         datePublished:2017-04-11T00:00:00Z
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            Gastric cancer
            IGF2BP3
            miR-34a
            Cancer Research
            Oncology
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      headline:IGF2BP3 functions as a potential oncogene and is a crucial target of miR-34a in gastric carcinogenesis
      description:Gastric cancer (GC) is one of the frequent causes of cancer-related death in eastern Asian population. IGF2BP2 lists in the top rank up-regulated genes in GC, but its functional role is unclear. The expression of IGF2BP3 in GC cell lines and primary samples was examined by qRT-PCR and Western blot. The biological role of IGF2BP3 was revealed by a series of functional in vitro studies. Its regulation by microRNAs (miRNAs) was predicted by TargetScan and confirmed by luciferase assays and rescue experiments. IGF2BP3 ranked the No.1 of the up-regulated genes by expression microarray analysis in GC cell lines. The expression level of IGF2BP3 was observed in GC tissues comparing with non-tumorous gastric epitheliums. The up-regulated IGF2BP3 expression was associated with poor disease specific survival. IGF2BP3 knockdown significantly inhibited cell proliferation and invasion. Apart from copy number gain, IGF2BP3 has been confirmed to be negatively regulated by tumor-suppressive miRNA, namely miR-34a. The expression of miR-34a showed negative correlation with IGF2BP3 mRNA expression in primary GC samples and more importantly, re-overexpression of IGF2BP3 rescued the inhibitory effect of miR-34a. We compressively revealed the oncogenic role of IGF2BP3 in gastric tumorigenesis and confirmed its activation is partly due to the silence of miR-34a. Our findings identified useful prognostic biomarker and provided clinical translational potential.
      datePublished:2017-04-11T00:00:00Z
      dateModified:2017-04-11T00:00:00Z
      pageStart:1
      pageEnd:14
      license:http://creativecommons.org/publicdomain/zero/1.0/
      sameAs:https://doi.org/10.1186/s12943-017-0647-2
      keywords:
         Gastric cancer
         IGF2BP3
         miR-34a
         Cancer Research
         Oncology
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      isPartOf:
         name:Molecular Cancer
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         name:BioMed Central
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            type:ImageObject
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      author:
            name:Yuhang Zhou
            affiliation:
                  name:The Chinese University of Hong Kong
                  address:
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                     type:PostalAddress
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                  name:Institute of Digestive Disease, The Chinese University of Hong Kong
                  address:
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                  name:Li Ka Shing Institute of Health Science, The Chinese University of Hong Kong
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                     name:Department of Anaesthesia and Intensive Care, The Chinese University of Hong Kong, Hong Kong, People’s Republic of China
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            name:Alfred S. L. Cheng
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                     name:Shenzhen Research Institute, The Chinese University of Hong Kong, Shenzhen, People’s Republic of China
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            type:Person
            name:Jun Yu
            affiliation:
                  name:Institute of Digestive Disease, The Chinese University of Hong Kong
                  address:
                     name:Partner State Key Laboratory of Digestive Disease, Institute of Digestive Disease, The Chinese University of Hong Kong, Hong Kong, People’s Republic of China
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                  name:The Chinese University of Hong Kong
                  address:
                     name:Department of Medicine and Therapeutics, The Chinese University of Hong Kong, Hong Kong, People’s Republic of China
                     type:PostalAddress
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            type:Person
            name:Ka Fai To
            affiliation:
                  name:The Chinese University of Hong Kong
                  address:
                     name:Department of Anatomical and Cellular Pathology, State Key Laboratory in Oncology in South China, Prince of Wales Hospital, The Chinese University of Hong Kong, Hong Kong, People’s Republic of China
                     type:PostalAddress
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                  name:Institute of Digestive Disease, The Chinese University of Hong Kong
                  address:
                     name:Partner State Key Laboratory of Digestive Disease, Institute of Digestive Disease, The Chinese University of Hong Kong, Hong Kong, People’s Republic of China
                     type:PostalAddress
                  type:Organization
                  name:Li Ka Shing Institute of Health Science, The Chinese University of Hong Kong
                  address:
                     name:Sir Y.K. Pao Cancer Center, Li Ka Shing Institute of Health Science, The Chinese University of Hong Kong, Hong Kong, People’s Republic of China
                     type:PostalAddress
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                  name:Shenzhen Research Institute, The Chinese University of Hong Kong
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                     name:Shenzhen Research Institute, The Chinese University of Hong Kong, Shenzhen, People’s Republic of China
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            name:Wei Kang
            affiliation:
                  name:The Chinese University of Hong Kong
                  address:
                     name:Department of Anatomical and Cellular Pathology, State Key Laboratory in Oncology in South China, Prince of Wales Hospital, The Chinese University of Hong Kong, Hong Kong, People’s Republic of China
                     type:PostalAddress
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                  name:Institute of Digestive Disease, The Chinese University of Hong Kong
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                     name:Partner State Key Laboratory of Digestive Disease, Institute of Digestive Disease, The Chinese University of Hong Kong, Hong Kong, People’s Republic of China
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            address:
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               type:PostalAddress
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            address:
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            name:Institute of Digestive Disease, The Chinese University of Hong Kong
            address:
               name:Partner State Key Laboratory of Digestive Disease, Institute of Digestive Disease, The Chinese University of Hong Kong, Hong Kong, People’s Republic of China
               type:PostalAddress
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            address:
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            address:
               name:Shenzhen Research Institute, The Chinese University of Hong Kong, Shenzhen, People’s Republic of China
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      name:Sir Y.K. Pao Cancer Center, Li Ka Shing Institute of Health Science, The Chinese University of Hong Kong, Hong Kong, People’s Republic of China
      name:Department of Anatomical and Cellular Pathology, State Key Laboratory in Oncology in South China, Prince of Wales Hospital, The Chinese University of Hong Kong, Hong Kong, People’s Republic of China
      name:Partner State Key Laboratory of Digestive Disease, Institute of Digestive Disease, The Chinese University of Hong Kong, Hong Kong, People’s Republic of China
      name:Sir Y.K. Pao Cancer Center, Li Ka Shing Institute of Health Science, The Chinese University of Hong Kong, Hong Kong, People’s Republic of China
      name:Shenzhen Research Institute, The Chinese University of Hong Kong, Shenzhen, People’s Republic of China
      name:Department of Anatomical and Cellular Pathology, State Key Laboratory in Oncology in South China, Prince of Wales Hospital, The Chinese University of Hong Kong, Hong Kong, People’s Republic of China
      name:Partner State Key Laboratory of Digestive Disease, Institute of Digestive Disease, The Chinese University of Hong Kong, Hong Kong, People’s Republic of China
      name:Partner State Key Laboratory of Digestive Disease, Institute of Digestive Disease, The Chinese University of Hong Kong, Hong Kong, People’s Republic of China
      name:Department of Anatomical and Cellular Pathology, State Key Laboratory in Oncology in South China, Prince of Wales Hospital, The Chinese University of Hong Kong, Hong Kong, People’s Republic of China
      name:Department of Gastroenterology, The Affiliated Drum Tower Hospital of Nanjing University, Medical School, Nanjing, People’s Republic of China
      name:Partner State Key Laboratory of Digestive Disease, Institute of Digestive Disease, The Chinese University of Hong Kong, Hong Kong, People’s Republic of China
      name:Department of Anaesthesia and Intensive Care, The Chinese University of Hong Kong, Hong Kong, People’s Republic of China
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      name:Department of Medicine and Therapeutics, The Chinese University of Hong Kong, Hong Kong, People’s Republic of China
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