Xuzhou Maternal and Child Health Hospital, Xuzhou Medical University, Xuzhou, 221000, China.
College of Medicine, University of Illinois at Chicago, Chicago, Illinois, USA.
Biochem Genet. 2022 Feb;60(1):303-314. doi: 10.1007/s10528-021-10098-z. Epub 2021 Jun 30.
Cervical cancer (CC) is one of the most frequently diagnosed tumors in female. miR-122 has been proved to be dominant in CC. The particular role of miR-122 in CC is unclear. Thus, we attempted to investigate the prognostic role of miR-122 in CC. We used the database of Kaplan-Meier curve plot. Growth and apoptosis of C33A cells were detected by CCK-8, colony formation assay, transwell assays and flow cytometry analysis. The target gene of miR-122 was identified using bioinformatics, q-PCR, western blot and luciferase assay. It showed that CC patients with overexpression of miR-122 have a better prognosis in the Kaplan-Meier plot database analysis. Overexpressed miR-122 inhibited the malignant growth and induced apoptosis of CC. miR-122 targeting of RAD21 cohesin complex component (RAD21) was identified using bioinformatics, Q-PCR, western blot and luciferase assay analyses. Moreover, we found miR-122 conduct its functions via RAD21 via the PI3K/AKT signaling pathway. Importantly, overexpression of RAD21 restored the roles of miR-122 in CC. Our data suggested that miR-122 could block malignant growth and promoted apoptosis by targeting RAD21 in CC. Our finding indicates miR-122 could potentially participate in the pathogenesis and be a biomarker or the potential therapeutic target of CC.
宫颈癌(CC)是女性最常见的肿瘤之一。miR-122 已被证明在 CC 中占主导地位。miR-122 在 CC 中的特定作用尚不清楚。因此,我们试图研究 miR-122 在 CC 中的预后作用。我们使用 Kaplan-Meier 曲线图数据库。通过 CCK-8、集落形成测定、Transwell 测定和流式细胞术分析检测 C33A 细胞的生长和凋亡。使用生物信息学、q-PCR、western blot 和荧光素酶测定鉴定 miR-122 的靶基因。结果表明,在 Kaplan-Meier 图谱数据库分析中,miR-122 过表达的 CC 患者预后较好。过表达的 miR-122 抑制 CC 的恶性生长并诱导细胞凋亡。使用生物信息学、q-PCR、western blot 和荧光素酶测定分析鉴定 miR-122 靶向 RAD21 凝聚复合物成分(RAD21)。此外,我们发现 miR-122 通过 PI3K/AKT 信号通路通过 RAD21 发挥其功能。重要的是,RAD21 的过表达恢复了 miR-122 在 CC 中的作用。我们的数据表明,miR-122 可以通过靶向 RAD21 阻断 CC 中的恶性生长并促进凋亡。我们的发现表明,miR-122 可能参与 CC 的发病机制,并可能成为 CC 的生物标志物或潜在治疗靶点。