腺性膀胱炎发病率有上升趋势，易复发、有恶性进展潜能，目前其调控机制尚不明确。申请人前期通过基因芯片、生物信息学技术分析发现lncRNA GCAT1在腺性膀胱炎组织中表达下调，与PTEN有一段相同的能和miR-155-5p互补结合的碱基序列，而pathway分析提示PTEN可能参与调控PI3K/Akt信号轴。随后细胞实验证实，GCAT1在腺性膀胱炎细胞中低表达，且表达水平与miR-155-5p呈负相关，与PTEN呈正相关。据此我们提出假设：GCAT1通过ceRNA机制竞争性结合miR-155-5p，调控PTEN/PI3K/Akt信号通路，从而影响腺性膀胱炎的进展。本项目拟通过双荧光素酶报告基因、RIP和原位杂交等方法，从体内、体外和临床病理等角度来验证这一设想，以阐明上述调控网络为核心的腺性膀胱炎进展机制，为其诊治提供新的靶点。

Glandular cystitis, a disease with increasing incidence and recurrence rate, has the potential of malignant progression, but its pathogenesis remains unclear. Through microarray screening and bioinformatics analysis, we found that the expression of lncRNA GCAT1 in glandular cystitis tissues was lower than in normal bladder tissues. It has the same base sequence as PTEN and the sequence is complementary to miR-155-5p. Pathway analysis suggested that PTEN may be involved in the regulation of PI3K/Akt signaling axis. Our preliminary experiments confirmed that GCAT1 was low expressed in glandular cystitis, and the expression level was negatively correlated with miR-155-5p, and positively correlated with PTEN. Based on above, we hypothesize that GCAT1 regulates PTEN/PI3K/Akt signaling pathway by competitively binding miR-155-5p through ceRNA mechanism, thereby affecting the development of glandular cystitis. This project intends to verify this hypothesis by in vivo, in vitro and clinicopathological methods through dual luciferase reporter, RIP and in situ hybridization, in order to clarify the epigenetic mechanism with ceRNA regulatory network and provide a new biomarker and therapeutic target for the diagnosis and treatment of glandular cystitis.