HORMONAL EFFECTS ON CELL-PROLIFERATION IN A HUMAN ERYTHROLEUKEMIA CELL-LINE (K562)

  • 1 January 1980
    • journal article
    • research article
    • Vol. 56  (5) , 886-891
Abstract
The hormonal responsiveness of human K562 erythroleukemia cells was investigated, using a serum-substituted in vitro clonogenic assay. Dexamethasone inhibited colony formation by the K562 cells, and the inhibitory effect could be reversed by progesterone (10-6 M). Fluoxymesterone caused a prominent enhancement of K562 colony growth, whereas estriol had no effect. Stimulation by triiodothyronine was maximal at 10-7 M, and the thyroid effect could be abrogated by the .beta.2-adrenergic antagonist butoxamine in equimolar concentrations. Using standard tissue culture conditions, the .beta.-adrenergic agent isoproterenol, but not the .alpha.-catecholamine phenylephrine, enhanced the proliferation of K562 cells. When K562 cells were grown under hormone-depleted conditions, they developed responsiveness to phenylephrine and were no longer stimulated by isoproterenol. DbcAMP [dibutyuyl cAMP] and prostaglandins of the E series also caused K562 colony enhancement. Prostaglandin F2.alpha. had no effect on cell proliferation. Insulin was an effective stimulant of colony formation of K562 cells, as were human growth hormone and ovine prolactin. Bovine growth hormone had no effect. K562 is apparently an erythroid line. K562 cells respond to endocrine hormones in a manner analogous to normal erythroid progenitors.