LncRNA在肿瘤发生发展中作用关键。我们前期在卵巢癌和乳腺癌中均发现新型LncRNA Lnc-OC1有促癌功能，包括在肿瘤中上调，敲减Lnc-OC1抑制细胞增殖、浸润迁移、干性、肿瘤生长并促进凋亡。机制上我们发现Lnc-OC1可与蛋白激酶PDPK1结合并可能介导PI3K/AKT信号进而激活有氧糖酵解通路。本项目拟进一步研究：1）Lnc-OC1在卵巢癌、乳腺癌中的完整作用；2）Lnc-OC1与PDPK1的相互作用及Lnc-OC1与PDPK1互作对PI3K/AKT信号进而对有氧糖酵解的调节作用；3）Lnc-OC1与PDPK1结合所介导PI3K/AKT信号和有氧糖酵解在卵巢癌、乳腺癌中作用；4）通过商业化组织芯片检测Lnc-OC1、PDPK1、p-PDPK1、PI3K/AKT信号和有氧糖酵解通路相关基因的相关性。最终为Lnc-OC1作为卵巢癌和乳腺癌诊断、治疗与预后靶标提供坚实基础。

Long non-coding RNAs (LncRNAs) play a critical role in tumor initiation and development. In our previous studies, we identified the oncogenic role of a novel LncRNA, Lnc-OC1, in ovarian and breast cancer. Lnc-OC1 was upregulated in tumors. Silence of Lnc-OC1 suppressed cancer cell proliferation, invasion, migration, stemness, xenograft growth and induced cellular apoptosis. Mechanistically, we found that Lnc-OC1 potentially bound to protein kinase PDPK1 to modulate the PI3K/AKT signaling pathway and then aerobic glycolysis. In this project, we aim to: 1）systematically elucidate the function of Lnc-OC1 in the formation and development of ovarian and breast cancer; 2）confirm the interaction of Lnc-OC1 with PDPK1 and its role in the activation of PI3K/AKT signaling and aerobic glycolysis; 3) determine the role of Lnc-OC1 and PDPK1 interaction-regulated PI3K/AKT signaling and aerobic glycolysis in ovarian and breast cancer formation and development; 4) examine the relationship among Lnc-OC1, PDPK1, p-PDPK1, PI3K/AKT- and aerobic glycolysis-associated genes, clinicopathological characteristics and molecular subtyping in commercial ovarian and breast cancer tissues. Our work may afford a new diagnostic and prognostic marker and one effective therapeutic target for ovarian and breast cancer.