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宽坪杂岩是连接北秦岭构造带和华北板块的重要岩石-构造单元之一，其物质组成和变质变形特征可为探讨北秦岭构造带与华北板块构造关系及演化提供重要证据。本文在已有研究基础上，对宝鸡-眉县-洛南一带宽坪变碎屑岩进行了系统的岩石学、矿物学和碎屑锆石U-Pb年代学研究。结果表明，宽坪碎屑岩最年轻碎屑锆石年龄峰值为~550Ma，最主要碎屑锆石年龄集中区为~2.5Ga和1.0~0.9Ga，次要年龄集中区为1.3~1.0Ga和850~750Ma。通过与周缘可能物源区的年代学特征对比揭示，宽坪碎屑岩物源主要来自北秦岭新元古代花岗岩与秦岭岩群副片麻岩，部分来自南秦岭和扬子板块北缘新元古代花岗岩以及太古宙基底岩系，缺乏华北板块物质；宽坪碎屑岩的碎屑锆石年龄谱特征与南侧的二郎坪碎屑岩近乎一致，暗示两者可能形成于同一沉积盆地。相平衡模拟结果显示，洛南红土岭宽坪杂岩含石榴子石石英片岩记录了顺时针P-T演化轨迹，峰期变质条件为P=7.17~7.92kbar，T=557~563℃，形成于大陆碰撞过程。结合前人报道宽坪杂岩~440Ma的变质年龄，我们认为在早志留世时期宽坪和二郎坪沉积盆地闭合，北秦岭构造带与华北板块碰撞形成现今的构造格局，在此之前北秦岭构造带与华北板块不具有亲缘性。

Background: LncRNA hotair is an oncogene that involves in the progression of several cancers. Previously we and others have reported that hotair promotes glioblastoma progression by regulating cell cycle. However, further mechanism still needs to be explored. The wnt/b-catenin signaling pathway is a crucial factor in the development of many cancers. B-catenin is a nuclear transcription factor that regulates multiple genes involved in cell proliferation, survival and EMT that contribute to glioma development. Methods: Positive correlation genes of hotair were picked up from CGGA (Chinese Glioma Genome Atlas) database by bioinformatics analysis. Real Time PCR is used to test the mRNA expression levels in U87 cells and astrocytes. Western blot is emplored to determine PKM2 expression after knocking down hotair. Further more, and nude mouse glioma intracranial model is employed to examine in vivo impact of hotair on GBM. Results: Hotair is a cell cycle related lncRNA as previously reported. Bioinformatics analysis indicated that various genes play important roles on cell cycle are positively correlated with hotair. Theses genes might be the executors of hotair on cell cycle regulating. We constructed a top 18 hotair-related genes network by connectivity. To test the hypothesis, we knock down hotair expression in U87 cells, and found out that FOXM1, CCNA2, CEP55, CENEP, CCNB2, HMMR, NCAPG, NUSAP were down-regulated significantly. In addition, overexpression of hotair in astrocytes could upregulate the mRNA of those genes. To further explore the regulatory mechanism, we analyed the promoter of these hotair-regulated genes and found out b-catenin/TCF4 binding site on all of them. This indicated that hotair might upregulate cell cycle associated genes through b-catenin/TCF4 pathway. FH535 is an inhibitor of wnt/b-catenin. The mRNA expression of these genes could be suppressed by FH535 treatment, which confirms the promoter analysis. It is reported that PKM2 could promote b-catenin nuclear translocation. Interestingly, we found out that binding site of miR-330 exists on both of hotair and PKM2 mRNA. Knocking-down of hotair inhibited PKM2 mRNA and protein expression in U87, U87vIII, U251 and LN229 cells. Further more, hotair siRNA could inhibit glioma growth in vivo. Conclusion: Our data indicated that hotair promotes glioma cell cycle through a b-catenin mediated mRNA network, and hotair could be a a biomarker and therapeutic target in glioblastoma. Meanwhile, there are still a lot of work to be done. Citation Format: Qixue Wang, Kai Huang, Yu Ren, Yunfei Wang, Bingcong Zhou, Yanli Tan, Chuan Fang, Jie Li, Chunsheng Kang. Hotair promotes glioma cell cycle through a b-catenin mediated mRNA network. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 997.