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Investigation of the Roles of Non-neuronal Acetylcholine in Chronic Myeloid Leukemic Cells and their Erythroid or Megakaryocytic Differentiated Lines

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dc.contributor.authorAYDIN OMAY, BANU
dc.contributor.authorsAydin, Banu; Cabadak, Hulya; Goren, M. Zafer
dc.date.accessioned2022-03-12T22:24:36Z
dc.date.available2022-03-12T22:24:36Z
dc.date.issued2018
dc.description.abstractBackground: Many studies suggested that Acetylcholine (ACh) might serve as an autocrine/paraerine growth factor in several types of tumors or tumor cell lines. High levels of Acetylcholinesterase (AChE) activity have been reported in primary brain tumors, ovarian, colon and lung tumors. Objectives: The role of cholinergic signaling needs to be clarified in in leukemia. Method: K562 cells were derived from a chronic myelogenous leukemia patient during blast crisis serving as pluripotent hematopoietic stein cells. K562 cells were incubated with various cholinergic agonists or antagonists to investigate the role of ACh in different differentiated cell lines. Results: Our experiments showed that AChE activity was increased in response to ACh in undifferentiated K562 cells, but in the erythroid differentiated K562 cells a high concentration of ACh (1 mM) decreased the AChE activity. ACh failed to elevate the AChE activity in the megakaryocytic differentiated K562 cells. An AChE inhibitor, eserine, also suppressed the AChE activity in a concentration-dependent manner. Choline uptake inhibition by hemicholinium did increase the AChE activity but not in the erythroid differentiated K562 DOS cell line. Likewise, megakaryocytic differentiated K562 cells also displayed a similar pattern. Vesamicole, a vesicular choline uptake inhibitor, produced similar results. Curare, a nicotinic antagonist, elevated the cell counts of the megakaryocytic differentiated cells. Conclusion: Our findings may suggest excess extracellular ACh will decrease the cell growth in undifferentiated and megakaryocytic differentiated K562 cell lines through nicotinic type cholinoceptors.
dc.identifier.doi10.2174/1871520618666180406123154
dc.identifier.eissn1875-5992
dc.identifier.issn1871-5206
dc.identifier.pubmed29623856
dc.identifier.urihttps://hdl.handle.net/11424/234800
dc.identifier.wosWOS:000456470300008
dc.language.isoeng
dc.publisherBENTHAM SCIENCE PUBL LTD
dc.relation.ispartofANTI-CANCER AGENTS IN MEDICINAL CHEMISTRY
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.subjectAcetylcholinesterase
dc.subjectcurare
dc.subjectvesamicole
dc.subjecthemicholinium 3
dc.subjectK562 cells
dc.subjectcholinergic
dc.subjectCHOLINERGIC SYSTEM
dc.subjectCLINICAL-ASPECTS
dc.subjectBIOLOGICAL-SYSTEMS
dc.subjectK562 CELLS
dc.subjectEXPRESSION
dc.subjectRELEASE
dc.subjectPROLIFERATION
dc.subjectLYMPHOCYTES
dc.subjectINDUCTION
dc.subjectAPOPTOSIS
dc.titleInvestigation of the Roles of Non-neuronal Acetylcholine in Chronic Myeloid Leukemic Cells and their Erythroid or Megakaryocytic Differentiated Lines
dc.typearticle
dspace.entity.typePublication
local.avesis.ida475b752-90ea-46ae-91a0-b229cf3f2ef8
local.import.packageSS17
local.indexed.atWOS
local.indexed.atSCOPUS
local.indexed.atPUBMED
local.journal.numberofpages8
local.journal.quartileQ3
oaire.citation.endPage1447
oaire.citation.issue10
oaire.citation.startPage1440
oaire.citation.titleANTI-CANCER AGENTS IN MEDICINAL CHEMISTRY
oaire.citation.volume18
relation.isAuthorOfPublicationaf9e48cc-cef6-4af2-bdb7-5b424aadfc2b
relation.isAuthorOfPublication.latestForDiscoveryaf9e48cc-cef6-4af2-bdb7-5b424aadfc2b

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