http://purl.uniprot.org/citations/29054762 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/29054762 | http://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/29054762 | http://purl.org/dc/terms/identifier | "doi:10.1016/j.gene.2017.10.046"xsd:string |
http://purl.uniprot.org/citations/29054762 | http://purl.uniprot.org/core/author | "Zhou Y."xsd:string |
http://purl.uniprot.org/citations/29054762 | http://purl.uniprot.org/core/author | "Lin Y.P."xsd:string |
http://purl.uniprot.org/citations/29054762 | http://purl.uniprot.org/core/author | "Wang H.B."xsd:string |
http://purl.uniprot.org/citations/29054762 | http://purl.uniprot.org/core/author | "Ding B.Z."xsd:string |
http://purl.uniprot.org/citations/29054762 | http://purl.uniprot.org/core/date | "2018"xsd:gYear |
http://purl.uniprot.org/citations/29054762 | http://purl.uniprot.org/core/name | "Gene"xsd:string |
http://purl.uniprot.org/citations/29054762 | http://purl.uniprot.org/core/pages | "56-65"xsd:string |
http://purl.uniprot.org/citations/29054762 | http://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/29054762 | http://purl.uniprot.org/core/volume | "644"xsd:string |
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