LncRNA以多种方式在肿瘤中发挥促癌或抑癌作用。我们前期发现CRYM-AS1在胶质母细胞瘤中高表达并发挥癌基因功能,但其机制并不明确。进一步分析发现CRYM-AS1能够与CRYM蛋白结合，显著延长CRYM的半衰期促进蛋白稳定性，上调CRYM-AS1抑制蛋白酶体活性。综上提出，CRYM-AS1通过泛素-蛋白酶体途径抑制CRYM的泛素化从而稳定蛋白质半衰期促进表达。同时，下调CRYM-AS1、CRYM引起细胞脂肪酸表达变化，MPEA显示下调CRYM-AS1、CRYM与脂肪酸代谢密切相关，且下调两者都促进脂肪酸β-氧化的限速酶CPT1B的表达，因此提出“CRYM-AS1通过CRYM调控AMPK/ ACC1/CPT1B通路促进胶质母细胞瘤脂肪酸氧化代谢”。通过本项目研究不仅可以阐明CRYM-AS1调控CRYM表达的机制，同时初步阐明CRYM-AS1通过CRYM参与脂肪酸代谢,发挥癌基因的功能。

LncRNA plays important roles in the pathophysiology of the diseases,including cancer,and regulates the malignant characteristic of tumor cells in various ways.In the preliminary study, we found that CRYM-AS1 is high expressed and function as an oncogene,but the mechanism has not been reported.Further analysis revealed that CRYM-AS1 can bind to CRYM protein,significantly extending the half-life of CRYM and promotes protein stability, Overexpression of CRYM-AS1 can inhibit proteasome activity,Based on these empirical and literature analysis,we hypothesize that CRYM-AS1 inhibits the ubiquitination of CRYM through the ubiquitin-proteasome pathway, stabilizing the half-life of the protein and promoting its expression.We also found that knockdown of CRYM-AS1 and CRYM induced changes in the expression of cellular fatty acids,CRYM-AS1 and CRYM were synergistically involved in the regulation of fatty acids metabolism by metabolite pathway enrichment analysis, and knockdown of CRYM-AS1 and CRYM can promote the expression of carnitine palmitoyltransferase 1B(CPT1B),so we hypothesized that "CRYM-AS1 regulates AMPK /ACC1 / CPT1B pathway through CRYM to promote fatty acid oxidation in glioblastoma".By this project, we will not only elucidate the mechanism of CRYM-AS1 regulating CRYM,but also preliminarily elucidate the role of CRYM-AS1 and CRYM in fatty acid metabolism and its oncogene function in glioblastoma.