Please use this identifier to cite or link to this item: http://cmuir.cmu.ac.th/jspui/handle/6653943832/75554
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dc.contributor.authorKhin Thenu Ayeen_US
dc.contributor.authorSakornniya Wattanapongpitaken_US
dc.contributor.authorBenjamaporn Supawaten_US
dc.contributor.authorSuchart Kothanen_US
dc.contributor.authorChatchanok Udomtanakunchaien_US
dc.contributor.authorSingkome Timaen_US
dc.contributor.authorJie Panen_US
dc.contributor.authorMontree Tungjaien_US
dc.date.accessioned2022-10-16T07:00:43Z-
dc.date.available2022-10-16T07:00:43Z-
dc.date.issued2021-10-01en_US
dc.identifier.issn17912431en_US
dc.identifier.issn1021335Xen_US
dc.identifier.other2-s2.0-85114422809en_US
dc.identifier.other10.3892/or.2021.8178en_US
dc.identifier.urihttps://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=85114422809&origin=inwarden_US
dc.identifier.urihttp://cmuir.cmu.ac.th/jspui/handle/6653943832/75554-
dc.description.abstractLeukemia is a common malignancy affecting humans worldwide. Pirarubicin (Pira) is one of the anticancer agents used for the treatment of leukemia. Although Pira is effective, drug resistance may develop in cancer cells exposed to this drug, whereas the combination of natural products with Pira may help to overcome this problem. The aim of the present study was to focus on the effect of gallic acid (GA) on the anticancer activity of Pira in K562 leukemia cells and K562/doxorubicin (Dox)-resistant leukemia cells in order to investigate the possible underlying mechanisms. The cell viability, mitochondrial activity, mitochondrial membrane potential (ΔΨm) and ATP levels were assessed in living K562 and K562/Dox cancer cells following treatment with GA/Pira combination, GA alone or Pira alone. P-glycoprotein-mediated efflux of Pira was determined in GA-treated K562/Dox cancer cells. The results demonstrated that GA/Pira combination decreased cell viability, mitochondrial activity, ΔΨm and ATP levels in K562 and K562/Dox cancer cells in a GA concentration-dependent manner compared with non-treated or Pira-treated cells. GA inhibited P-glycoprotein-mediated efflux of Pira in GA-treated K562/Dox cancer cells. Therefore, GA enhanced the anticancer effect of Pira on K562 and K562/Dox cancer cells through cellular energy status impairment, and was able to reverse drug resistance in living K562/Dox cancer cells by inhibiting the function of P-glycoprotein.en_US
dc.subjectBiochemistry, Genetics and Molecular Biologyen_US
dc.subjectMedicineen_US
dc.titleGallic acid enhances pirarubicin-induced anticancer in living K562 and K562/Dox leukemia cancer cells through cellular energetic state impairment and P-glycoprotein inhibitionen_US
dc.typeJournalen_US
article.title.sourcetitleOncology Reportsen_US
article.volume46en_US
article.stream.affiliationsShandong Normal Universityen_US
article.stream.affiliationsChiang Mai Universityen_US
Appears in Collections:CMUL: Journal Articles

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