恶性黑色素瘤是高恶性、早转移、死亡率高的肿瘤。研究显示BRAFV600E突变与黑色素瘤发生密切相关，但机制不清。我们前期发现，BRAFV600E突变的黑色素瘤细胞中，长链非编码RNA BANCR （BRAF-activated non-protein coding RNA）与磷酸戊糖通路关键酶G6PD都高表达。结合生物信息学分析，提出BRAFV600E突变可通过其调控的BANCR，影响G6PD，使肿瘤细胞发生代谢重编程的假说。为此，本研究在临床样本、细胞模型（BANCR缺失、过表达等）和动物模型中，观察BRAFV600E/BANCR/G6PD通路与患者预后的关系；进一步干预BRAFV600E/BANCR/G6PD通路，观察肿瘤细胞的糖代谢重编程、代谢酶的改变以及对肿瘤细胞增殖的抑制作用。本课题以靶向人类黑色素瘤的代谢为切入点，从LncRNA角度，为黑色素瘤的治疗提供潜在的靶点和和理论依据。

Malignant melanoma (MM), is a highly malignant tumor with early metastasis and high mortality. Recent studies have shown that BRAFV600E mutation closely associated with melanoma, but the mechanism has not been well elucidated. Our previous experiments revealed that BANCR（BRAF-activated non-protein coding RNA）is highly expressed in melanoma cells, accompanied with the abnormal expression of pentose phosphate pathway (PPP) key metabolic enzyme G6PD. With bioinformatics analysis, we propose the hypothesis that BRAFV600E mutation could interfere G6PD by mediation of lncRNA BANCR regulated by BRAFV600E, and make tumor cell reprogramming. To prove that, we investigate the relationship between BRAFV600E/BANCR/G6PD pathway with prognosis in the MM clinical samples. Furthermore,we will establish the cell model (the stable melanoma cell line with deletion or overexpression of BANCRR, ect.) and animal models.Then,we intervene the BRAFV600E/BANCR/G6PD pathway, and observe the influence on glucose metabolism of tumor cell metabolism reprogramming, effect on metabolic enzyme, and inhibition on proliferation of tumor cell. This study is designed to focus on human MM metabolism and offer a potential target and evidence for MM treatment around LncRNA.