Cholera holotoxin produces both stimulation and inhibition of the growth of different cell populations. These opposite effects were both attributed to the enzymatic activity of the subunit A that activates adenylate cyclase, increasing the intracellular level of cAMP. We observed that the B subunit of cholera toxin produced by itself an inhibition of the 'in vitro' growth of two murine leukemia cell lines (L1210 limphoid leukemia and WEHI-3B myelomonocytic leukemia). The sensitivity of WEHI-3B cells towards cholera toxin was about 5000-times higher than that of the L1210 cells, whereas the two leukemias showed an identical sensitivity to the B subunit (IC50 = 5.10(-10) M for L1210 and 10(-10) M for WEHI-3B). The inhibition produced by the B subunit was neutralized by GM1 and in a minor degree by type II gangliosides. The two leukemias showed a remarkable difference in their gangliosides contents (L1210 cells contained GM1 (80.6%) and GM2 (19.4%), while WEHI-3B cells contained GM1 (28.2%), Fuc-GM1 (44.9%) and a band (26.9%) with a chromatographic mobility between GD1a and GD1b). The inhibition could be explained by a competitive mechanism between the B subunit and some autocrine factor binding GM1-containing receptors. Our data strengthen the suggestion to consider gangliosides as very important pleiotropic biomodulators.

Pessina, A., Mineo, E., Masserini, M., Neri, M., Cocuzza, C. (1989). Inhibition of murine leukemia (WEHI-3B and L1210) proliferation by cholera toxin B subunit. BIOCHIMICA ET BIOPHYSICA ACTA, 1013(3), 206-11.

Inhibition of murine leukemia (WEHI-3B and L1210) proliferation by cholera toxin B subunit

MASSERINI, MASSIMO ERNESTO;COCUZZA, CLEMENTINA ELVEZIA
1989

Abstract

Cholera holotoxin produces both stimulation and inhibition of the growth of different cell populations. These opposite effects were both attributed to the enzymatic activity of the subunit A that activates adenylate cyclase, increasing the intracellular level of cAMP. We observed that the B subunit of cholera toxin produced by itself an inhibition of the 'in vitro' growth of two murine leukemia cell lines (L1210 limphoid leukemia and WEHI-3B myelomonocytic leukemia). The sensitivity of WEHI-3B cells towards cholera toxin was about 5000-times higher than that of the L1210 cells, whereas the two leukemias showed an identical sensitivity to the B subunit (IC50 = 5.10(-10) M for L1210 and 10(-10) M for WEHI-3B). The inhibition produced by the B subunit was neutralized by GM1 and in a minor degree by type II gangliosides. The two leukemias showed a remarkable difference in their gangliosides contents (L1210 cells contained GM1 (80.6%) and GM2 (19.4%), while WEHI-3B cells contained GM1 (28.2%), Fuc-GM1 (44.9%) and a band (26.9%) with a chromatographic mobility between GD1a and GD1b). The inhibition could be explained by a competitive mechanism between the B subunit and some autocrine factor binding GM1-containing receptors. Our data strengthen the suggestion to consider gangliosides as very important pleiotropic biomodulators.
Articolo in rivista - Articolo scientifico
Granulocytes; Female; Animals; Leukemia L1210; Colony-Stimulating Factors; Hematopoietic Stem Cells; Peptide Fragments; Gangliosides; Tumor Cells, Cultured; Mice; Cholera Toxin; Macrophages; Cell Division; Leukemia, Experimental; G(M1) Ganglioside
English
206-11
Pessina, A., Mineo, E., Masserini, M., Neri, M., Cocuzza, C. (1989). Inhibition of murine leukemia (WEHI-3B and L1210) proliferation by cholera toxin B subunit. BIOCHIMICA ET BIOPHYSICA ACTA, 1013(3), 206-11.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/10281/34677
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