Department of Obstetric and Gynecology, Renmin Hospital of Wuhan University, Wuhan 430000, China.
Department of Gynecology, The First Affiliated Hospital of Xinjiang Medical University, Urumchi 830001, China.
Biomed Res Int. 2022 Jul 28;2022:5793912. doi: 10.1155/2022/5793912. eCollection 2022.
Cervical cancer (CC) is the second main reason of cancer-related deaths in women around the world. Long intergenic nonprotein coding RNA 707, which is known as LINC00707, has been elucidated to facilitate the progression of multifarious tumors, but how it may exert functions in CC has not been elucidated yet. By using quantitative real-time RT-PCR (RT-qPCR), we identified the expression pattern LINC00707 may possess in CC. Loss-of-function assays including Cell Counting Kit-8 (CCK-8), colony formation, and transferase-mediated dUTP nick-end labeling (TUNEL) assays were taken to verify the effects of LINC00707 inhibition on CC cell proliferation and apoptosis. The downstream RNAs were selected through bioinformatics prediction, and their interaction with LINC00707 was verified through mechanism assays including the luciferase reporter assay, RNA pull-down assay, and RNA immunoprecipitation (RIP) assay. According to results, LINC00707 was upregulated in CC cells, and LINC00707 insufficiency inhibited cell proliferation while facilitating cell apoptosis. MicroRNA (miRNA) miR-374c-5p interacted with LINC00707, and syndecan-4 (SDC4) was verified to be the downstream target gene. Data of rescue assays proved that LINC00707 could promote CC cell malignancy via the miR-374c-5p/SDC4 axis, which revealed a potential treatment option for CC.
宫颈癌(CC)是全球女性癌症相关死亡的第二大主要原因。长链非编码 RNA 707,又称为 LINC00707,已经被阐明可以促进多种肿瘤的进展,但它在 CC 中如何发挥作用尚未阐明。通过使用实时定量 RT-PCR(RT-qPCR),我们确定了 LINC00707 在 CC 中可能具有的表达模式。通过细胞计数试剂盒-8(CCK-8)、集落形成和转移酶介导的 dUTP 缺口末端标记(TUNEL)测定等功能丧失测定来验证 LINC00707 抑制对 CC 细胞增殖和凋亡的影响。通过生物信息学预测选择下游 RNA,并通过包括荧光素酶报告测定、RNA 下拉测定和 RNA 免疫沉淀(RIP)测定在内的机制测定来验证它们与 LINC00707 的相互作用。结果表明,LINC00707 在 CC 细胞中上调,LINC00707 不足抑制细胞增殖,同时促进细胞凋亡。miRNA(miR-374c-5p)与 LINC00707 相互作用,并且验证了 syndecan-4(SDC4)是下游靶基因。挽救测定的数据证明,LINC00707 可以通过 miR-374c-5p/SDC4 轴促进 CC 细胞恶性转化,这为 CC 提供了一种潜在的治疗选择。