Department of Biological Sciences, University of Notre Dame, Notre Dame, IN, 46556-0369, USA.
Department of Biological Sciences, University of Notre Dame, Notre Dame, IN, 46556-0369, USA.
Exp Cell Res. 2022 Jun 1;415(1):113106. doi: 10.1016/j.yexcr.2022.113106. Epub 2022 Mar 18.
Invasive melanoma is an aggressive form of skin cancer with high incidence of mortality. The process of tumor invasion is a crucial primary step in the metastatic cascade, yet the mechanisms involved are still under investigation. Here we document a critical role for MLK3 (MAP3K11) in the regulation of melanoma cell invasion. We report the unexpected finding that cellular loss of MLK3 in melanoma cells promotes cell invasion. Cellular depletion of MLK3 expression results in the hyperactivation of ERK, which is linked to the formation of a BRAF/Hsp90/Cdc37 protein complex. ERK hyperactivation leads to enhanced phosphorylation and inactivation of GSK3β and the stabilization of c-Jun and JNK activity. Blocking of ERK and JNK signaling as well as Hsp90 activity downstream of MLK3-silencing significantly reduces melanoma invasion. Furthermore, ERK activation in the aforementioned context is coupled to MT1-MMP transcription as well as the TOM1L1-dependent localization of the membrane protease to invadopodia at the invasive front. These studies provide critical insight into the mechanisms that couple MLK3 loss with BRAF hyperactivation and its consequence on melanoma invasion.
侵袭性黑色素瘤是一种具有高死亡率的侵袭性皮肤癌。肿瘤侵袭的过程是转移级联的关键初始步骤,但涉及的机制仍在研究中。在这里,我们记录了 MLK3(MAP3K11)在调节黑色素瘤细胞侵袭中的关键作用。我们报告了一个意想不到的发现,即黑色素瘤细胞中 MLK3 的细胞缺失会促进细胞侵袭。MLK3 表达的细胞耗竭导致 ERK 的过度激活,这与 BRAF/Hsp90/Cdc37 蛋白复合物的形成有关。ERK 的过度激活导致 GSK3β 的磷酸化和失活增强,以及 c-Jun 和 JNK 活性的稳定。阻断 ERK 和 JNK 信号以及 MLK3 沉默下游的 Hsp90 活性可显著降低黑色素瘤的侵袭性。此外,上述情况下的 ERK 激活与 MT1-MMP 的转录以及膜蛋白酶在侵袭前沿向依赖 TOM1L1 的侵袭小体的定位相关。这些研究为 MLK3 缺失与 BRAF 过度激活及其对黑色素瘤侵袭的影响之间的偶联机制提供了重要的见解。