AI Article Synopsis
- The study examines how hemin affects the inhibition of erythroid differentiation in K562 cells, particularly when influenced by a monoclonal antibody targeting the human transferrin receptor.
- In the absence of hemin, the antibody suppresses hemoglobin production triggered by treatments like butyric acid or 5-azacytidine.
- However, when hemin is present, a hemin-resistant K562 cell line can produce hemoglobin even with the antibody present, indicating that hemin may help overcome the inhibitory effects of the antibody on iron uptake and hemoglobin synthesis.
Article Abstract
We have studied the effects of hemin on the inhibition of K562 cell erythroid differentiation mediated by a monoclonal antibody to the human transferrin receptor. In the absence of hemin, the monoclonal antibody 42/6 suppresses the increase of hemoglobin accumulation induced by butyric acid or 5-azacytidine (5-azaCR). In contrast, in the presence of hemin, the hemin-resistant K562(h) cell line is induced to hemoglobin production by treatment with 5-azaCR even in the presence of the monoclonal antibody to human transferrin receptor. The results obtained suggest (1) that the human leukemic K562 cells treated with monoclonal antibodies to human transferrin receptor might retain molecular properties similar to those found in erythroid cells from subjects affected by alterations of iron metabolism, and (2) that hemin might allow hemoglobin synthesis in erythroid cells whose iron uptake is inhibited by monoclonal antibodies to human transferrin receptors.
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