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dc.contributor.authorAhmadian, N
dc.contributor.authorPashaei-Asl, R
dc.contributor.authorSamadi, N
dc.contributor.authorRahmati-Yamchi, M
dc.contributor.authorRashidi, MR
dc.contributor.authorAhmadian, M
dc.contributor.authorEsmaeili, M
dc.contributor.authorSalamat, F
dc.contributor.authorBesharat, S
dc.contributor.authorJoshaghani, HR
dc.date.accessioned2018-08-26T05:05:40Z
dc.date.available2018-08-26T05:05:40Z
dc.date.issued2016
dc.identifier.urihttp://dspace.tbzmed.ac.ir:8080/xmlui/handle/123456789/39377
dc.description.abstractBACKGROUND Hesa-A is a natural compound with anticancer properties. The exact mechanism of its action in esophageal cancer is not clear, yet. The aim of this study was to evaluate the cell toxicity effect of Hesa-A on the esophageal carcinoma cell lines, KYSE-30, and cell cycle genes expression. METHODS In this study, we tested cell toxicity with MTT (3-(4,5-Dimethylthiazol-2-yl)-2,5-Diphenyltetrazolium Bromide) assay and flow cytometry to evaluatet he cell cycle arrest. Real time polymerase chain reaction was used to assess the expression of P53, P16, P21, cyclin D1, and cyclin B1 genes. RESULTS Our results showed that Hesa-A is effective in the expression of cell cycling check point proteins. Hesa-A induced an arrest in G2 phase of esophageal cell cycle. The levels of P53 (>13 times), P21 (>21 times), P16, cyclin B1, and cyclin D1 genes were increased 48 hours after Hesa-A treatment. CONCLUSION P21 and P16 expression were the potential mechanisms for G2 arrest of KYSE-30 esophageal cancer cell line by Hesa-A.
dc.language.isoEnglish
dc.relation.ispartofMiddle East journal of digestive diseases
dc.titleHesa-A Effects on Cell Cycle Signaling in Esophageal Carcinoma Cell Line.
dc.typearticle
dc.citation.volume8
dc.citation.issue4
dc.citation.spage297
dc.citation.epage302
dc.citation.indexPubmed
dc.identifier.DOIhttps://doi.org/10.15171/mejdd.2016.39


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