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首页> 外文期刊>Journal of Cellular Physiology >Methylselenol generated from selenomethionine by methioninase downregulates integrin expression and induces caspase-mediated apoptosis of B16F10 melanoma cells.
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Methylselenol generated from selenomethionine by methioninase downregulates integrin expression and induces caspase-mediated apoptosis of B16F10 melanoma cells.

机译：Methylselenol产生硒代蛋氨酸methioninase会使整合素表达和B16F10细胞凋亡caspase-mediated黑色素瘤细胞。

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摘要

Melanoma is a highly metastatic cancer resistant to current chemotherapeutic and radiotherapeutic approaches. Several studies have shown that interactions between cancer cells and the extracellular matrix (ECM) are critical for the survival and invasion of metastatic cancer cells. In this study, we examine the effects of methylselenol generated from selenomethionine (SeMet) by methioninase (METase) on cell proliferation, adhesion, and expression of integrins in murine melanoma B16F10 cells, which are metastatic in the lungs of syngeneic C57BL/6J mice. Combined treatment with SeMet-METase decreased the expression of integrins alpha(4), beta(1), alpha(nu), and beta(3), and inhibited melanoma-ECM adhesion. Caspase-mediated apoptosis was induced following loss of cell adherence. Phosphorylation of focal adhesion kinase (FAK) and Akt, related to integrin-mediated survival, were decreased upon treatment with SeMet-METase while phosphorylation of p38, PKC-delta, and IkappaBalpha increased. In the presence of specific inhibitors of p38, PKC-delta, and NF-kappaB, expression of integrins and cell adhesion to ECM were maintained and cell apoptosis was prevented in SeMet-METase-treated melanoma cells. Treatment with caspase inhibitors restored cell viability and blocked poly (ADP-ribose) polymerase (PARP) cleavage, but did not restore integrin expression and cell adhesion to ECMs reduced by SeMet-METase. Based on these results, we propose that combined treatment with SeMet-METase induces caspase-mediated apoptosis in melanoma cells by altering integrin expression and adhesion. Furthermore, activation of p38, PKC-delta, and NF-kappaB is a prerequisite for the down-regulation of integrin expression, followed by detachment-mediated apoptosis.
机译：黑色素瘤是一种高度转移性癌耐药目前的化疗和放射疗法的方法。癌细胞和之间的相互作用细胞外基质(ECM)是至关重要的转移性肿瘤细胞的存活和入侵。在这项研究中,我们审查的影响methylselenol产生硒代蛋氨酸(SeMet) methioninase (METase)细胞的增殖、粘附和表达整合蛋白在小鼠黑色素瘤B16F10细胞,这种细胞转移性肺的同源的C57BL / 6 j老鼠。整合素α(4)的表达减少,β(1),α(ν)和β(3)和抑制melanoma-ECM附着力。细胞粘附是诱导后的损失。粘着斑激酶(FAK)的磷酸化一种蛋白激酶,integrin-mediated生存有关,减少SeMet-METase治疗虽然p38的磷酸化,PKC-delta,IkappaBalpha增加。p38的特定抑制剂,PKC-delta,NF-kappaB,整合蛋白的表达和细胞和细胞粘附ECM一直都是有效的细胞凋亡在SeMet-METase-treated阻止黑色素瘤细胞。保利恢复细胞活力和阻塞(ADP-ribose)聚合酶(PARP)乳沟,但所做的不恢复整合素的表达和细胞粘附ecm减少SeMet-METase。结果,我们建议治疗相结合SeMet-METase细胞凋亡caspase-mediated在黑素瘤细胞通过改变整合素的表达和附着力。PKC-delta, NF-kappaB是可敬的前提条件整合素表达的下调,其次是detachment-mediated细胞凋亡。

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