Isolation and characterization of a large soluble form of fibronectin that stimulates adhesion, spreading, and alignment of mouse erythroleukemia cells.

Fibronectin (FN) is a major component of the extracellular matrix which plays important roles in a variety of cellular processes including cell adhesion, and migration. The soluble cellular form of FN has a monomer molecular weight of approximately 250 kDa, and generally exists as a dimer of 500 kDa. We have isolated a different form of soluble FN from mouse breast cancer cell line SC115 conditioned medium (CM) and purified it to homogeneity as evidenced by both native polyacrylamide gel electrophoresis (PAGE) and sodium dodecyl sulfate PAGE.

Sequences of polycythemia-type Friend spleen focus-forming virus in clone-745-derived mouse erythroleukemia cells.

Friend leukemia virus complex consists of a replication-competent virus plus one of two replication-incompetent viruses, spleen focus-forming virus anemia virus or spleen focus-forming virus polycythemia virus. The replication-incompetent viruses induce rapid malignant transformation of erythroid precursor cells. Transformed cell lines from mice infected with the complex can be induced to undergo erythrodifferentiation in vitro.

The phosphatase inhibitors, orthovanadate and levamisole, inhibit induction of erythroid differentiation and abrogate the associated inhibition of glycolysis.

Alterations in protein tyrosine phosphate (PTP), lactate, and fructose 2,6-bisphosphate (F-2,6-P2) levels have been associated with induced MEL cell differentiation and commitment to terminal cell division (TCD). The possible relationships of perturbations in PTP metabolism and reduction in lactate formation during differentiation were investigated utilizing sodium orthovanadate, Na3VO4, primarily an inhibitor of PTP phosphatases, and levamisole, considered an alkaline phosphatase inhibitor. Both of these compounds were found to effectively inhibit the TCD-associated differentiation induced by DMSO, HMBA, and Na butyrate and to abrogate the differentiation-associated reduction in lactate accumulation due to these agents.

Dephosphorylation of Vav is associated with the induction of mouse erythroleukemia cell differentiation: effects of orthovanadate and levamisole.

Mouse erythroleukemia (MEL) cell erythroid differentiation induced by dimethyl sulfoxide or hexamethylene bisacetamide (HMBA) is accompanied by the production of hemoglobin, terminal cell division and decreases in lactate production and fructose 2,6-bisphosphate levels. A number of studies have suggested that decreases in the cellular level of protein phosphotyrosine content may play a role in MEL cell differentiation. In particular, it was shown that the expression of several protein tyrosine phosphatase genes accompany this process and that the transfection of one of these genes into MEL cells followed by its subsequent expression induced eythroid differentiation.

Induction of erythroid differentiation is associated with inhibition of glycolysis and a decrease in fructose 2,6-bisphosphate levels.

The fraction of glucose metabolized to lactate is dramatically reduced during erythroid differentiation of mouse erythroleukemia (MEL) cells induced by dimethyl sulfoxide (DMSO), hexamethylene bisacetamide (HMBA), or sodium butyrate treatment. In order to determine the mechanism of the reduction in lactate production, several enzymatic steps in glucose catabolism were investigated. No changes in glycolytic enzyme levels were found during differentiation that could account for the alteration in lactate production and alterations in pyruvate kinase activity are known not to occur during MEL cell differentiation.