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dc.contributor.authorMohammadian, F
dc.contributor.authorPilehvar-Soltanahmadi, Y
dc.contributor.authorAlipour, S
dc.contributor.authorDadashpour, M
dc.contributor.authorZarghami, N
dc.date.accessioned2018-08-26T04:58:54Z
dc.date.available2018-08-26T04:58:54Z
dc.date.issued2017
dc.identifier.urihttp://dspace.tbzmed.ac.ir:8080/xmlui/handle/123456789/38796
dc.description.abstractBackground Gastric carcinoma still remains the second most common cause of cancer mortality in the world. Chrysin, as a flavone, has showed cancer chemopreventive activity. The cellular and molecular mechanisms of chrysin in cancer cells have not been fully understood. Objective In this study, we investigate expression levels of let-7a, miR-9, mir-18a, miR-21, miR-22, miR-34a, miR-126 and mir-221 to describe the anti-cancer effects of chrysin. Materials and Methods The cytotoxic effects of chrysin were assessed using MTT assay. The effect of chrysin on the microRNAs expression was determined by qRT-PCR. Results The MTT results for different concentrations of chrysin at different times on the Gastric carcinoma cells showed that IC50 for chrysin was 68.24?آµM after 24?h of treatment. Expression analysis identified that miR-18, miR-21 and miR-221 were down regulated whereas let-7a, miR-9, miR-22, miR-34a and miR-126 were up regulated in Gastric carcinoma cell line (p<0.05). Conclusion Treatment with chrysin can alter the miRNAs expression and these findings might be an explanation for molecular mechanism of chrysin effect on gastric cancer.
dc.language.isoEnglish
dc.relation.ispartofDrug research
dc.subjectAntineoplastic Agents, Phytogenic
dc.subjectCell Line, Tumor
dc.subjectDown-Regulation
dc.subjectFlavonoids
dc.subjectGene Expression Regulation, Neoplastic
dc.subjectHumans
dc.subjectInhibitory Concentration 50
dc.subjectMicroRNAs
dc.subjectReverse Transcriptase Polymerase Chain Reaction
dc.subjectStomach Neoplasms
dc.subjectTime Factors
dc.subjectUp-Regulation
dc.titleChrysin Alters microRNAs Expression Levels in Gastric Cancer Cells: Possible Molecular Mechanism.
dc.typearticle
dc.citation.volume67
dc.citation.issue9
dc.citation.spage509
dc.citation.epage514
dc.citation.indexPubmed
dc.identifier.DOIhttps://doi.org/10.1055/s-0042-119647


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