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首页> 外文期刊>Biochemistry >Loss of Concurrent Regulation of the Expression of BIF-1, BAX, and Beclin-1 in Primary and Metastatic Melanoma
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Loss of Concurrent Regulation of the Expression of BIF-1, BAX, and Beclin-1 in Primary and Metastatic Melanoma

机译：BIF-1，BAX和BECLIN-1表达同时调节在原发性和转移性黑色素瘤中的表达

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摘要

Melanoma is one of the most aggressive and drug-resistant cancers. Despite novel promising therapeutic strategies, the prognosis of metastatic melanoma patients remains poor and it is often associated with high relapse rates. Endophilin B1, also known as BIF-1, is a multifunctional protein involved in several biological processes such as autophagy and apoptosis. BIF-1 promotes apoptosis through binding to BAX and its translocation to the mitochondrial outer membrane. On the other hand, BIF-1 can interact with Beclin-1 through UVRAG to promote autophagy. Several reports suggest an ambiguous role of BIF-1 in cancer development and progression. For example, it has been demonstrated that the expression of BIF-1 is reduced in both primary and metastatic melanoma and that the reduction of BIF-1 expression is associated with reduced overall survival of melanoma patients. Here we show that the expression of Beclin-1 and active form of BAX are also reduced in the melanoma patients. However, while we observed strong positive correlations between the expression of BIF-1 and Beclin-1 as well as between BIF-1 and BAX in benign nevi, these correlations were lost in the primary and metastatic melanoma cells. These data indicate disruption in the proximal molecular mechanisms which regulate expression of BIF-1, Beclin-1, and BAX in the primary and metastatic melanoma.
机译：黑色素瘤是最具侵略性和耐药性的癌症之一。尽管具有新颖的治疗策略，转移性黑素瘤患者的预后仍然差，而且往往与高复发率有关。 Endophilin B1，也称为BIF-1，是涉及若干生物过程的多功能蛋白，例如自噬和凋亡。 BIF-1通过与Bax结合并将其易位促进细胞凋亡，并将其易位与线粒体外膜结合。另一方面，BIF-1可以通过UVRAG与BECLIN-1相互作用以促进自噬。几份报告表明BIF-1在癌症发展和进展中的含糊不清作用。例如，已经证明了BIF-1的表达在一次和转移性黑色素瘤中减少，并且BIF-1表达的还原与黑素瘤患者的整体存活率有关。在这里，我们表明，在黑素瘤患者中也减少了BECLIN-1和活性形式的BAX的表达。然而，虽然我们观察到BIF-1和BECIN-1的表达与BIF-1和BAX在良性NEVI之间的表达之间存在强烈的正相关性，但在初级和转移性黑素瘤细胞中丢失了这些相关性。这些数据表示在初级和转移性黑色素瘤中调节BIF-1，BECLIN-1和BAX表达的近似分子机制中断。

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