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http://purl.uniprot.org/citations/29054762http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/29054762http://www.w3.org/2000/01/rdf-schema#comment"Luteolin is a flavonoid compound derived from Lonicera japonica Thunb, which has been reported to exert anticancer effects on different types of tumors. miRNAs are a kind of endogenous non-coding small RNAs, which involved in occurrence and development of multi cancer, including miR-34a. However, the relationship between miR-34a and luteolin's susceptibility to cancer cells still remains unclear. In this study, we explored the roles of miR-34a and the effects of luteolin on GC cells as well as the underlying mechanism of miR-34a in mediating the susceptibility of GC cell to luteolin. Retrospectively study revealed that miR-34a expression was downregulated in human primary GC tissues compared with non-tumor tissues and low miR-34a expression was associated with a significantly shorter overall survival and disease-free survival. MiR-34a overexpression could inhibit GC cells and induce G1 phase arrest via p53/p21 and MAPK /ERK pathways. Luteolin decreased viability of GC cells in a dose-dependent manner. Meanwhile, miR-34a was found to be markedly upregulated in GC cells induced by luteolin and decreased miR-34a level was found in the artificial luteolin-resistant GC cells. Upregulation of miR-34a in luteolin-resistant GC cell could enhance the sensibility of GC cells to luteolin. On the other hand, miR-34a inhibitor could partly counter the anticancer effect of luteolin. In a further assay, we also found that targeting miR-34a could mediate the susceptibility of mouse xenografts to luteolin. Subsequent study found that HK1 was a direct target of miR-34a and downregulated HK1 mRNA or protein levels were presented after miRNA-34a overexpression in GC cells. Moreover, HK1 protein levels was decreased after luteolin treatment and partly restored when co-treated with luteolin and miR-34a inhibitor. Downregulation of HK1 in luteolin-resistant GC cell could increase the cell's sensitivity to luteolin. Therefore, our findings firstly suggested that miR-34a could modulate the susceptibility of gastric cancer cell to luteolin via targeting HK1, potentially benefiting GC patients' treatment in the future."xsd:string
http://purl.uniprot.org/citations/29054762http://purl.org/dc/terms/identifier"doi:10.1016/j.gene.2017.10.046"xsd:string
http://purl.uniprot.org/citations/29054762http://purl.uniprot.org/core/author"Zhou Y."xsd:string
http://purl.uniprot.org/citations/29054762http://purl.uniprot.org/core/author"Lin Y.P."xsd:string
http://purl.uniprot.org/citations/29054762http://purl.uniprot.org/core/author"Wang H.B."xsd:string
http://purl.uniprot.org/citations/29054762http://purl.uniprot.org/core/author"Ding B.Z."xsd:string
http://purl.uniprot.org/citations/29054762http://purl.uniprot.org/core/date"2018"xsd:gYear
http://purl.uniprot.org/citations/29054762http://purl.uniprot.org/core/name"Gene"xsd:string
http://purl.uniprot.org/citations/29054762http://purl.uniprot.org/core/pages"56-65"xsd:string
http://purl.uniprot.org/citations/29054762http://purl.uniprot.org/core/title"MiR-34a, as a suppressor, enhance the susceptibility of gastric cancer cell to luteolin by directly targeting HK1."xsd:string
http://purl.uniprot.org/citations/29054762http://purl.uniprot.org/core/volume"644"xsd:string
http://purl.uniprot.org/citations/29054762http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/29054762
http://purl.uniprot.org/citations/29054762http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/29054762
http://purl.uniprot.org/uniprot/#_A0A994J753-mappedCitation-29054762http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/29054762
http://purl.uniprot.org/uniprot/#_B4DG62-mappedCitation-29054762http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/29054762
http://purl.uniprot.org/uniprot/#_A8K7J7-mappedCitation-29054762http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/29054762
http://purl.uniprot.org/uniprot/#_B1AR62-mappedCitation-29054762http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/29054762
http://purl.uniprot.org/uniprot/#_B3KRA9-mappedCitation-29054762http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/29054762
http://purl.uniprot.org/uniprot/#_B3KXY9-mappedCitation-29054762http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/29054762
http://purl.uniprot.org/uniprot/#_P78542-mappedCitation-29054762http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/29054762
http://purl.uniprot.org/uniprot/#_Q71V75-mappedCitation-29054762http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/29054762
http://purl.uniprot.org/uniprot/#_P19367-mappedCitation-29054762http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/29054762
http://purl.uniprot.org/uniprot/#_Q59FD4-mappedCitation-29054762http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/29054762
http://purl.uniprot.org/uniprot/#_Q99609-mappedCitation-29054762http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/29054762