Suppression of metastatic potential of high-metastatic Lewis lung carcinoma cells by vanadate, an inhibitor of tyrosine phosphatase, through inhibiting cell-substrate adhesion.

Invasion & metastasis Pub Date : 1996-01-01
K Takenaga
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Abstract

Treatment of high-metastatic Lewis lung carcinoma A11 cells with sodium orthovanadate, a phosphotyrosine phosphatase inhibitor, resulted in a dose- and time-dependent suppression of cell spreading on various extracellular matrix components such as Matrigel, fibronectin, laminin and type IV collagen, while the treatment did not significantly inhibit attachment of the cells to these substrates. Orthovanadate slightly and reversibly inhibited the in vitro cell growth of A11 cells, but the suppression of cell spreading was not directly due to the inhibition of cell growth. Orthovanadate-treated A11 cells showed reduced invasive ability in a reconstituted basement membrane invasion assay and experimental metastatic ability. Protein tyrosine phosphorylation level in A11 cells was elevated after treatment with orthovanadate. The increase in tyrosine phosphorylation level was partially diminished by the tyrosine kinase inhibitor ST638, concomitantly with restoration of the suppressed cell spreading as well as invasive and metastatic abilities. These results suggest that protein tyrosine phosphorylation influences invasive and metastatic potential of tumor cells possibly through regulating cell-substrate adhesion.

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酪氨酸磷酸酶抑制剂钒酸盐通过抑制细胞-底物粘附抑制高转移性Lewis肺癌细胞的转移潜能。
正钒酸钠(一种磷酸酪氨酸磷酸酶抑制剂)治疗高转移性Lewis肺癌A11细胞,导致细胞在各种细胞外基质成分(如Matrigel、纤维连接蛋白、层粘连蛋白和IV型胶原)上的扩散受到剂量和时间依赖的抑制,而该治疗并未显著抑制细胞对这些底物的附着。正钒酸盐对A11细胞的体外生长有轻微且可逆的抑制作用,但对细胞扩散的抑制不是直接由于对细胞生长的抑制。原钒酸盐处理的A11细胞在重建基底膜侵袭实验和实验转移能力中显示出侵袭能力降低。原钒酸盐处理后,A11细胞蛋白酪氨酸磷酸化水平升高。酪氨酸激酶抑制剂ST638部分地减少了酪氨酸磷酸化水平的增加,同时恢复了被抑制的细胞扩散以及侵袭和转移能力。这些结果表明蛋白酪氨酸磷酸化可能通过调节细胞-底物粘附来影响肿瘤细胞的侵袭和转移潜能。
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