Background: Many studies suggested that Acetylcholine (ACh) might serve as an autocrine/ paracrine
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 stem 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
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.