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Research Article Free access | 10.1172/JCI115210

Endothelin-1 is an autocrine/paracrine growth factor for human cancer cell lines.

M Shichiri, Y Hirata, T Nakajima, K Ando, T Imai, M Yanagisawa, T Masaki, and F Marumo

Department of Medicine, Tokyo Medical and Dental University, Japan.

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Department of Medicine, Tokyo Medical and Dental University, Japan.

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Department of Medicine, Tokyo Medical and Dental University, Japan.

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Department of Medicine, Tokyo Medical and Dental University, Japan.

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Department of Medicine, Tokyo Medical and Dental University, Japan.

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Department of Medicine, Tokyo Medical and Dental University, Japan.

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Department of Medicine, Tokyo Medical and Dental University, Japan.

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Department of Medicine, Tokyo Medical and Dental University, Japan.

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Published May 1, 1991 - More info

Published in Volume 87, Issue 5 on May 1, 1991
J Clin Invest. 1991;87(5):1867–1871. https://doi.org/10.1172/JCI115210.
© 1991 The American Society for Clinical Investigation
Published May 1, 1991 - Version history
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Abstract

We studied whether a novel vasoconstrictor peptide, endothelin-1 (ET-1), is synthesized by and released from human carcinoma cell lines, and whether ET-1 stimulates proliferation of these tumor cells. ET-1-like immunoreactivity was released from both HeLa and HEp-2 cells as a function of time. Reverse-phase HPLC of the conditioned media from HeLa cells revealed a major peak coeluting with standard ET-1. Northern blot analysis demonstrated the expression of mRNA for ET-1 precursor in both tumor cell lines. Both cell lines contained a single class of specific binding sites for ET-1. ET-1 dose-dependently induced increases in cytosolic free Ca2+ concentration in fura-2-loaded tumor cells, whose effect was completely abolished by chelating extracellular Ca2+ or by Ca(2+)-channel blocker. ET-1 stimulated proliferation of the quiescent cell lines in a dose-dependent manner, whose effect was inhibited by Ca(2+)-channel blocker. Polyclonal antibody for ET-1 inhibited proliferation of these cell lines, whereas nonimmune serum had no effect. These results demonstrate that ET-1 is synthesized by and released from human epithelial carcinoma cell lines, and that exogenous and endogenous ET-1 stimulates proliferation of the cells possibly through Ca2+ influx, suggesting its role as an autocrine/paracrine growth factor for certain tumor cells.

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