端粒酶是维持细胞端粒长度的重要途径,而端粒酶（hTERT）主要在人类胚胎干细胞及大部分肿瘤细胞中表达。干细胞分化过程中细胞失去端粒酶活性，而在癌症发生或者T细胞激活过程中又重新激活端粒酶的表达，这提示端粒酶的表达与细胞增殖能力紧密相关。目前对于控制端粒酶基因表达的机制尚不清楚。近期，Pol II停滞对基因表达的影响颇受研究人员的关注，它主要调控胚胎发育及刺激响应相关基因的表达及mRNA的剪接。hTERT是胚胎发育所必须的基因，也能够被诱导表达，同时受到mRNA剪接的调节。我们的前期结果表明，hTERT的表达可能受到Pol II 停滞的调节。本项目拟从Pol II停滞着手深入研究hTERT基因表达与细胞分裂增殖能力的关系，并深入探讨调控hTERT表达的分子机制，寻找控制端粒酶表达的关键因子。

Telomerase is the most important way to keep the telomere length. The telomerase activity can only be detected in embryonic stem cell and in most cancers because of its gene expression regulation. The coding gene for telomerase is hTERT, and its mRNA can undergo alternative splicing, resulting in different telomerase activity, which is considered one of the telomerase activity regulation pathway. The gene expression and alternative splicing regulation mechanism of hTERT is not well understood hitherto. Recently, Pol II stalling catched much attention for its role in transcription initiation and alternative splicing. It regulates genes involved in embryonic development and stimuli response, and hTERT happens to belonging these areas. Therefore, we planed to explore the role of Pol II stalling in hTERT gene expression and alternative splicing, trying to explain the telomerase gene gexpression regulation mechanism in a novel way.