Yessotoxins (YTXs) are algal toxins that can be accumulated in edible molluscs. YTX treatment of MCF-7 breast cancer cells causes the accumulation of a 100 kDa fragment of E-cadherin, which we have named ECRA(100). A relative decrease in the concentrations of intact E-cadherin did not accompany the accumulation of ECRA(100) in cytosoluble extracts of MCF-7 cells on the first day of YTX treatment, but a collapse of the E-cadherin system was detected after 2-5 days of treatment with the toxin. An analysis of the general structure of ECRA(100) revealed that it consists of an E-cadherin fragment lacking the intracellular domain of the protein. ECRA(100) was not released into culture media of YTX-treated cells. Accumulation of ECRA(100) was observed in other epithelial cells, such as human intestine Caco-2 and MDCK cells after treatment with YTX. In turn, YTX could not induce accumulation of fragments of other members of the cadherin family, such as N-cadherin in the PC 12 cell line and K-cadherin in sensitive cells (MCF-7, Caco-2, MDCK). The accumulation of a 100 kDa fragment of E-cadherin devoid of its intracellular domain induced by YTX was accompanied by reduced levels of beta- and gamma-catenins bound to E-cadherin, without a concomitant decrease in the total cytosoluble pools of beta- and gamma-catenins. Taken together, the results we obtained show that YTX causes the selective disruption of the E-cadherin-catenin system in epithelial cells, and raise some concern about the potential that an algal toxin found in seafood might disrupt the tumour suppressive functions of E-cadherin.

Selective disruption of the E-cadherin-catenin system by an algal toxin / Ronzitti, Giuseppe; Callegari, Federica; C., Malaguti; Rossini, Gian Paolo. - In: BRITISH JOURNAL OF CANCER. - ISSN 0007-0920. - STAMPA. - 90:(2004), pp. 1100-1107. [10.1038/sj.bjc.6601640]

Selective disruption of the E-cadherin-catenin system by an algal toxin

RONZITTI, Giuseppe;CALLEGARI, Federica;ROSSINI, Gian Paolo
2004

Abstract

Yessotoxins (YTXs) are algal toxins that can be accumulated in edible molluscs. YTX treatment of MCF-7 breast cancer cells causes the accumulation of a 100 kDa fragment of E-cadherin, which we have named ECRA(100). A relative decrease in the concentrations of intact E-cadherin did not accompany the accumulation of ECRA(100) in cytosoluble extracts of MCF-7 cells on the first day of YTX treatment, but a collapse of the E-cadherin system was detected after 2-5 days of treatment with the toxin. An analysis of the general structure of ECRA(100) revealed that it consists of an E-cadherin fragment lacking the intracellular domain of the protein. ECRA(100) was not released into culture media of YTX-treated cells. Accumulation of ECRA(100) was observed in other epithelial cells, such as human intestine Caco-2 and MDCK cells after treatment with YTX. In turn, YTX could not induce accumulation of fragments of other members of the cadherin family, such as N-cadherin in the PC 12 cell line and K-cadherin in sensitive cells (MCF-7, Caco-2, MDCK). The accumulation of a 100 kDa fragment of E-cadherin devoid of its intracellular domain induced by YTX was accompanied by reduced levels of beta- and gamma-catenins bound to E-cadherin, without a concomitant decrease in the total cytosoluble pools of beta- and gamma-catenins. Taken together, the results we obtained show that YTX causes the selective disruption of the E-cadherin-catenin system in epithelial cells, and raise some concern about the potential that an algal toxin found in seafood might disrupt the tumour suppressive functions of E-cadherin.
2004
90
1100
1107
Selective disruption of the E-cadherin-catenin system by an algal toxin / Ronzitti, Giuseppe; Callegari, Federica; C., Malaguti; Rossini, Gian Paolo. - In: BRITISH JOURNAL OF CANCER. - ISSN 0007-0920. - STAMPA. - 90:(2004), pp. 1100-1107. [10.1038/sj.bjc.6601640]
Ronzitti, Giuseppe; Callegari, Federica; C., Malaguti; Rossini, Gian Paolo
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11380/306676
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