LINC00702通过与EZH2相互作用抑制KLF2转录，从而加速卵巢癌进展。
LINC00702 accelerates the progression of ovarian cancer through interacting with EZH2 to inhibit the transcription of KLF2.
作者信息
Wang L, Ye T-Y, Wu H, Chen S-Y, Weng J-R, Xi X-W
机构信息
Department of Obstetrics and Gynecology, Shanghai General Hospital of Nanjing Medical University, Shanghai, China.
出版信息
Eur Rev Med Pharmacol Sci. 2019 Aug;23(3 Suppl):201-208. doi: 10.26355/eurrev_201908_18648.
OBJECTIVE
To clarify the role of LINC00702 in the progression of ovarian cancer (OC) and the potential mechanism.
PATIENTS AND METHODS
Expression level of LINC00702 in OC tissues and matched normal tissues was detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). LINC00702 level in OC cell lines was determined as well. The potential influences of LINC00702 on cellular behaviors of A2780 and HEY cells were evaluated. The subcellular distribution of LINC00702 in A2780 cells was examined. Through RNA immunoprecipitation (RIP) and Chromatin immunoprecipitation (ChIP) assay, the interaction among LINC00702, EZH2, and KLF2 was verified. The rescue experiments were conducted to elucidate the biological function of LINC00702/KLF2 axis in the progression of OC.
RESULTS
LINC00702 was upregulated in OC tissues and cell lines. Its level was much higher in OC with worse tumor stage and larger tumor size. The knockdown of LINC00702 attenuated the proliferative ability of A2780 and HEY cells. LINC00702 was mainly distributed in the cell nucleus. The knockdown of LINC00702 or EZH2 downregulated the KLF2 level in the OC cells. The transfection of LINC00702 markedly reduced the occupancy of KLF2 promoter on EZH2 and H3K27me3 relative to IgG. Finally, the knockdown of KLF2 could reverse the regulatory effect of LINC00702 in the proliferative ability of A2780 cells.
CONCLUSIONS
LINC00702 is upregulated in OC. It accelerates the progression of OC via interacting with EZH2 to inhibit the transcription of KLF2.
目的
阐明LINC00702在卵巢癌（OC）进展中的作用及潜在机制。
患者和方法
采用定量实时聚合酶链反应（qRT-PCR）检测OC组织及配对正常组织中LINC00702的表达水平。同时测定OC细胞系中LINC00702的水平。评估LINC00702对A2780和HEY细胞细胞行为的潜在影响。检测LINC00702在A2780细胞中的亚细胞分布。通过RNA免疫沉淀（RIP）和染色质免疫沉淀（ChIP）实验，验证LINC00702、EZH2和KLF2之间的相互作用。进行挽救实验以阐明LINC00702/KLF2轴在OC进展中的生物学功能。
结果
LINC00702在OC组织和细胞系中上调。在肿瘤分期较差和肿瘤体积较大的OC中其水平更高。敲低LINC00702可减弱A2780和HEY细胞的增殖能力。LINC00702主要分布在细胞核中。敲低LINC00702或EZH2可下调OC细胞中KLF2的水平。相对于IgG，转染LINC00702显著降低了KLF2启动子上EZH2和H3K27me3的占有率。最后，敲低KLF2可逆转LINC00702对A2780细胞增殖能力的调节作用。
结论
LINC00702在OC中上调。它通过与EZH2相互作用抑制KLF2的转录，从而加速OC的进展。
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