Department of Surgery, Weill Cornell Medical College, New York Presbyterian Hospital, New York, NY, USA.
Department of Medicine, Weill Cornell Medical College, New York Presbyterian Hospital, New York, NY, USA.
Sci Rep. 2022 Apr 2;12(1):5573. doi: 10.1038/s41598-022-08936-0.
It is critical to understand the molecular mechanisms governing the regulation of MITF, a lineage specific transcription factor in melanocytes and an oncogene in melanoma. We identified PPP6C, a serine/threonine phosphatase, as a key regulator of MITF in melanoma. PPP6C is the only recurrently mutated serine/threonine phosphatase across all human cancers identified in sequencing studies and the recurrent R264C mutation occurs exclusively in melanoma. Using a zebrafish developmental model system, we demonstrate that PPP6C expression disrupts melanocyte differentiation. Melanocyte disruption was rescued by engineering phosphomimetic mutations at serine residues on MITF. We developed an in vivo MITF promoter assay in zebrafish and studied the effects of PPP6C(R264C) on regulating MITF promoter activity. Expression of PPP6C(R264C) cooperated with oncogenic NRAS(Q61K) to accelerate melanoma initiation in zebrafish, consistent with a gain of function alteration. Using a human melanoma cell line, we examined the requirement for PPP6C in proliferation and MITF expression. We show that genetic inactivation of PPP6C increases MITF and target gene expression, decreases sensitivity to BRAF inhibition, and increases phosphorylated MITF in a BRAF(V600E) mutant melanoma cell line. Our data suggests that PPP6C may be a relevant drug target in melanoma and proposes a mechanism for its action.
了解调控 MITF 的分子机制至关重要,MITF 是黑素细胞中一种谱系特异性转录因子,也是黑色素瘤中的癌基因。我们鉴定出 PPP6C 是黑色素瘤中 MITF 的关键调节因子,它是丝氨酸/苏氨酸磷酸酶家族中唯一在所有人类癌症测序研究中反复突变的磷酸酶,而 R264C 突变则仅发生在黑色素瘤中。利用斑马鱼发育模型系统,我们证明 PPP6C 的表达会破坏黑素细胞分化。通过对 MITF 丝氨酸残基进行磷酸模拟突变的工程设计,可挽救黑素细胞的破坏。我们在斑马鱼中开发了一种体内 MITF 启动子检测,研究了 PPP6C(R264C)对调节 MITF 启动子活性的影响。PPP6C(R264C)的表达与致癌性 NRAS(Q61K)协同作用,加速了斑马鱼黑色素瘤的起始,这与功能获得性改变一致。我们利用人类黑色素瘤细胞系研究了 PPP6C 在增殖和 MITF 表达中的作用。我们发现 PPP6C 的遗传失活增加了 MITF 和靶基因的表达,降低了 BRAF 抑制剂的敏感性,并增加了 BRAF(V600E)突变黑色素瘤细胞系中磷酸化 MITF 的水平。我们的数据表明 PPP6C 可能是黑色素瘤中一个相关的药物靶点,并提出了其作用机制。