Suppression of adhesion-induced protein tyrosine phosphorylation decreases invasive and metastatic potentials of B16-BL6 melanoma cells by protein tyrosine kinase inhibitor genistein.

Invasion & metastasis Pub Date : 1997-01-01
C Yan, R Han
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Abstract

Protein tyrosine kinase (PTK) appears to be involved in the activation of signaling during cell attachment to and spreading on extracellular matrix (ECM) in the metastatic cascade. To verify the assumption that PTK inhibitors might impair ECM signaling and prevent cancer metastasis, the highly metastatic B16-BL6 mouse melanoma cells were exposed to the PTK inhibitor genistein for 3 days. The ability of the cells to invade through reconstituted basement membrane (Matrigel) and to establish experimental pulmonary metastatic foci in C57BL/6 mice decreased after genistein exposure. The genistein-treated cells were also prevented from attaching to Matrigel and spread extremely poorly on the ECM substratum. Immunoblot analysis showed that tyrosine phosphorylation of a 125-kD protein in response to cell spreading on Matrigel was suppressed in the genistein-treated cells. Adhesion-induced protein tyrosine phosphorylation represents the earlier and specific event in the activation of ECM signaling, so this result implied ECM signaling was impaired in the treated cells. With immunofluorescence microscopy, the adhesion-induced tyrosine phosphorylated proteins were located at the pericytoplasms of well-spread cells, but not at the periphery of poorly spread genistein-treated cells. Therefore, this paper suggests that genistein might impair ECM signaling and subsequently prevent cancer cells from spreading well and invading or establishing metastasis through the suppression of adhesion-induced protein tyrosine phosphorylation. PTKs and adhesion-induced protein tyrosine phosphorylation might play a role in the control of invasion and metastasis.

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蛋白酪氨酸激酶抑制剂染料木黄酮抑制粘附诱导的蛋白酪氨酸磷酸化可降低B16-BL6黑色素瘤细胞的侵袭和转移潜力。
蛋白酪氨酸激酶(PTK)似乎参与了转移级联中细胞附着和在细胞外基质(ECM)上扩散过程中的信号激活。为了验证PTK抑制剂可能损害ECM信号并阻止癌症转移的假设,我们将高度转移的B16-BL6小鼠黑色素瘤细胞暴露于PTK抑制剂染料木素3天。染料木素暴露后,C57BL/6小鼠肺细胞通过重组基底膜(matrix)侵袭和建立实验性肺转移灶的能力下降。染料木素处理的细胞也被阻止附着在基质上,并且在ECM基质上的扩散非常差。免疫印迹分析显示,在染料木素处理的细胞中,响应细胞在Matrigel上扩散的125-kD蛋白酪氨酸磷酸化被抑制。黏附诱导的蛋白酪氨酸磷酸化代表了ECM信号激活的早期和特异性事件,因此这一结果表明在处理的细胞中ECM信号被破坏。在免疫荧光显微镜下,黏附诱导的酪氨酸磷酸化蛋白位于扩散良好的细胞的周细胞质上,而不在扩散不良的染料木素处理的细胞的周围。因此,本文认为染料木素可能通过抑制粘附诱导的蛋白酪氨酸磷酸化,破坏ECM信号传导,从而阻止癌细胞良好的扩散、侵袭或建立转移。PTKs和黏附诱导的蛋白酪氨酸磷酸化可能在控制侵袭和转移中发挥作用。
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