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Title:
IGF2BP3 functions as a potential oncogene and is a crucial target of miR-34a in gastric carcinogenesis | Molecular Cancer
Description:
Background 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. Method 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. Results 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. Conclusion 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.
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Keywords {š}
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 {āļø}
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 {ā}
- Insulin-like growth factor 2 mRNA-binding proteins (IGF2BPs): post-transcriptional drivers of cancer progression?
- Mir-34: a new weapon against cancer?
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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
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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
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Gastric cancer
IGF2BP3
miR-34a
Cancer Research
Oncology
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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, Peopleās 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, Peopleās Republic of China
name:Partner State Key Laboratory of Digestive Disease, Institute of Digestive Disease, The Chinese University of Hong Kong, Hong Kong, Peopleās Republic of China
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name:Partner State Key Laboratory of Digestive Disease, Institute of Digestive Disease, The Chinese University of Hong Kong, Hong Kong, Peopleās 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, Peopleās Republic of China
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name:Partner State Key Laboratory of Digestive Disease, Institute of Digestive Disease, The Chinese University of Hong Kong, Hong Kong, Peopleās 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, Peopleās Republic of China
name:Shenzhen Research Institute, The Chinese University of Hong Kong, Shenzhen, Peopleās Republic of China
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