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SP1 诱导的长链非编码 RNA DANCR 促进卵巢癌细胞的增殖和侵袭。

SP1-induced lncRNA DANCR contributes to proliferation and invasion of ovarian cancer.

机构信息

Department of Gynecology, Affiliated Hospital of Chengde Medical University, Chengde City, Hebei Province, China.

出版信息

Kaohsiung J Med Sci. 2021 May;37(5):371-378. doi: 10.1002/kjm2.12316. Epub 2020 Oct 22.

Abstract

Transcription factor SP1 could manipulate pathways involved in ovarian cancer progression. LncRNAs are involved in SP1-mediated tumorigenesis. LncRNA DANCR could promote metastasis of ovarian cancer. However, the regulatory function and involvement of SP1-induced lncRNA DANCR in ovarian cancer remain elusive. Data from this study showed that SP1 was up-regulated in ovarian cancer tissues and cells (CAOV3, SKOV3, A2780), and SP1 could bind to the promoter region of DANCR through chromatin immunoprecipitation and leuciferase activity assays. Therefore, DANCR was transcriptionally induced by SP1 in ovarian cancer tissues and cells (CAOV3, SKOV3, A2780). Functionally, reduced expression of DANCR suppressed cell viability, migration and invasion of CAOV3, while enhanced DANCR expression contributed to SKOV3 growth. Over-expression of SP1 reversed the suppressive effects of DANCR interference on ovarian cancer progression. In conclusion, SP1-induced DANCR contributed to oncogenic potential of ovarian cancer, suggesting a promising therapeutic target for ovarian cancer.

摘要

转录因子 SP1 可以操纵与卵巢癌进展相关的途径。LncRNA 参与 SP1 介导的肿瘤发生。LncRNA DANCR 可促进卵巢癌细胞转移。然而,SP1 诱导的 lncRNA DANCR 在卵巢癌中的调节功能和作用仍不清楚。本研究数据显示,SP1 在卵巢癌组织和细胞(CAOV3、SKOV3、A2780)中上调,并且 SP1 可以通过染色质免疫沉淀和荧光素酶活性测定结合到 DANCR 的启动子区域。因此,DANCR 在卵巢癌组织和细胞(CAOV3、SKOV3、A2780)中由 SP1 转录诱导。功能上,DANCR 的表达降低抑制了 CAOV3 的细胞活力、迁移和侵袭,而增强的 DANCR 表达有助于 SKOV3 的生长。SP1 的过表达逆转了 DANCR 干扰对卵巢癌进展的抑制作用。总之,SP1 诱导的 DANCR 有助于卵巢癌的致癌潜力,提示其可能成为卵巢癌的治疗靶点。

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