Department of Reproductive Medicine, Liaocheng People's Hospital, NO.67, Dongchang West Road, Liaocheng City, 252000, Shandong Province, China.
Department of Obstetrics and Gynecology, Liaocheng Tird People's Hospital, Liaocheng, Shandong, China.
J Ovarian Res. 2022 Jan 4;15(1):3. doi: 10.1186/s13048-021-00931-9.
Circular RNA (circRNA) has been shown to be involved in the regulation of human disease progression, including ovarian cancer (OC). Circ_0078607 was found to participate in OC progression. But its function and mechanism in OC deserve further exploration.
The expression levels of circ_0078607, salt-inducible kinase 1 (SIK1) and microRNA (miR)-32-5p were examined by qRT-PCR. And the protein expression levels of SIK1, metastasis marker and apoptosis marker were determined using western blot analysis. EDU staining, colony formation assay, transwell assay and flow cytometry were used to detect the proliferation, migration, invasion and apoptosis of cells. Moreover, dual-luciferase reporter assay was employed to verify the interaction between miR-32-5p and circ_0078607 or SIK1. Xenograft models were constructed to perform in vivo experiments.
Circ_0078607 and SIK1 were downregulated in OC tissues and cells. Overexpressed circ_0078607 and SIK1 could inhibit OC cell proliferation, migration, invasion, and promote apoptosis. MiR-32-5p could be sponged by circ_0078607, and its overexpression could reverse the suppressive effect of circ_0078607 on OC progression. Furthermore, SIK1 was a target of miR-32-5p, and circ_0078607 could regulate SIK1 by sponging miR-32-5p. The inhibitory effect of circ_0078607 on OC progression also could be reversed by SIK1 silencing. In vivo experiments showed that circ_0078607 reduced OC tumorigenesis by regulating the miR-32-5p/SIK1 axis.
Circ_0078607 could serve as a sponge of miR-32-5p to regulate SIK1 expression, thereby inhibiting OC progression.
环状 RNA（circRNA）已被证明参与了人类疾病的进展，包括卵巢癌（OC）。circ_0078607 被发现参与 OC 的进展。但它在 OC 中的功能和机制仍有待进一步探索。
通过 qRT-PCR 检测 circ_0078607、盐诱导激酶 1（SIK1）和 microRNA（miR）-32-5p 的表达水平。通过 Western blot 分析检测 SIK1、转移标记物和凋亡标记物的蛋白表达水平。EDU 染色、集落形成实验、Transwell 实验和流式细胞术用于检测细胞的增殖、迁移、侵袭和凋亡。此外，双荧光素酶报告基因实验用于验证 miR-32-5p 与 circ_0078607 或 SIK1 的相互作用。构建异种移植模型进行体内实验。
circ_0078607 和 SIK1 在 OC 组织和细胞中下调。过表达 circ_0078607 和 SIK1 可抑制 OC 细胞的增殖、迁移、侵袭，并促进凋亡。miR-32-5p 可被 circ_0078607 海绵吸附，其过表达可逆转 circ_0078607 对 OC 进展的抑制作用。此外，SIK1 是 miR-32-5p 的靶基因，circ_0078607 可通过海绵吸附 miR-32-5p 来调节 SIK1。circ_0078607 对 OC 进展的抑制作用也可通过 SIK1 沉默逆转。体内实验表明，circ_0078607 通过调节 miR-32-5p/SIK1 轴减少 OC 肿瘤发生。
circ_0078607 可作为 miR-32-5p 的海绵体调节 SIK1 表达，从而抑制 OC 进展。
