胶质瘤极易复发且对化疗药物不敏感。以组蛋白乙酰化转移酶为靶点的小分子抑制剂HATi II具有明显的抗肿瘤活性，其机制尚不明确。HATi II诱导细胞凋亡时uc001pxz.1显著上调，过表达pxz.1后能够引起胶质瘤细胞凋亡。软件预测及实验提示BLID为pxz.1的潜在靶标，我们猜测pxz.1通过BLID调控细胞凋亡，从而介导HATi II的抗肿瘤作用。鉴此，本研究拟阐明pxz.1在HATi II诱导细胞凋亡中的具体作用；以BLID为机制主线，研究BLID的功能，以挽救策略探讨 pxz.1 与BLID的可能的调控机制；进一步通过荧光素酶报告基因和CHART技术，揭示pxz.1对BLID的调控作用；结合临床胶质瘤标本及原代细胞验证pxz.1对BLID的调控机制。迄今未见pxz.1参与细胞凋亡的报道，研究将为胶质瘤细胞凋亡机制提供新思路，为小分子靶向的肿瘤治疗新策略提供实验依据和理论基础。

Glioma is easy to relapse and not sensitive to chemotherapy drugs. We found that a new small histone acetylation transferase inhibitor HATi II has a significant antitumor effect, while the mechanism was unclear. LncRNA uc001pxz.1 was significantly up-regulated when glioma cells were treated with HATi II. Overexpress pxz. 1 could induce cell apoptosis in vitro. Bioinformatic analysis and experiments suggested BLID was candidate target gene to pxz.1. It suggests that pxz.1 maybe regulate cell apoptosis induced by HATi II through BLID, thus mediating the antitumor activity. Based on these data, we plan to investigate the role and function of pxz.1 in glioma apoptosis and detailed regulatory mechanism of the interaction between pxz.1 and BLID through in vitro and in vivo experiments. Furthermore, we will further evaluate the mechanism of pxz.1 and BLID in glioma tissues and primary culture cells. So far there is no report about lncRNA uc001pxz.1 in glioma’s apoptosis. This study will show us a new thought to combat glioma, thereby providing experimental evidence and theoretical basis for establishment a new strategy in cancer therapy.