Li Cui, Li Yujuan, Zhang Yuying, Yan Hua, Huang Chengxiang
Department of Gynecology, Linyi Central Hospital, Linyi, Shandong 276400, P.R. China.
Exp Ther Med. 2021 Oct;22(4):1184. doi: 10.3892/etm.2021.10618. Epub 2021 Aug 16.
Cervical cancer (CC) is a type of gynecological malignancy that poses a significant threat to females. The aim of the present study was to examine the role of long intergenic non-protein coding RNA 1123 (LINC01123) and its underlying molecular mechanism in the development of CC. mRNA expression levels of LINC01123 and microRNA (miR)-361-3p in CC tissue samples and cell lines were evaluated using reverse transcription-quantitative PCR. Cell viability, migration and invasion were detected using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, wound healing and Transwell assays. Moreover, a xenograft tumor model was established for elucidating the influence of LINC01123 knockdown on tumor growth . A dual-luciferase reporter assay was used to confirm the association between LINC01123 and miR-361-3p, and miR-361-3p and tetraspanin 1 (TSPAN1). Western blot analysis was used to determine TSPAN1 protein expression. LINC01123 expression was upregulated and miR-361-3p expression was reduced in CC tissue samples and cell lines. Knockdown of LINC01123 inhibited cell viability, migration and invasion , and suppressed tumor growth . Furthermore, LINC01123 targeted miR-361-3p and negatively regulated miR-361-3p expression. Overexpression of miR-361-3p inhibited cell viability, migration and invasion in HeLa and CaSki cells. Additionally, miR-361-3p targeted TSPAN1 and negatively regulated TSPAN1 expression. Inhibition of miR-361-3p and overexpression of TSPAN1 reversed the effect of LINC01123 knockdown on cell proliferation, migration and invasion in HeLa cells. Knockdown of LINC01123 inhibited cell proliferation, migration and invasion via miR-361-3p/TSPAN1 regulation in CC, which may present an effective target for treatment of CC.
宫颈癌（CC）是一种对女性构成重大威胁的妇科恶性肿瘤。本研究的目的是探讨长链基因间非编码RNA 1123（LINC01123）在CC发生发展中的作用及其潜在分子机制。采用逆转录定量PCR评估CC组织样本和细胞系中LINC01123和微小RNA（miR）-361-3p的mRNA表达水平。使用3-（4,5-二甲基噻唑-2-基）-2,5-二苯基四氮唑溴盐、伤口愈合实验和Transwell实验检测细胞活力、迁移和侵袭能力。此外，建立异种移植肿瘤模型以阐明敲低LINC01123对肿瘤生长的影响。采用双荧光素酶报告基因实验来证实LINC01123与miR-361-3p以及miR-361-3p与四跨膜蛋白1（TSPAN1）之间的关联。使用蛋白质免疫印迹分析来测定TSPAN1蛋白表达。在CC组织样本和细胞系中，LINC01123表达上调，miR-361-3p表达降低。敲低LINC01123可抑制细胞活力、迁移和侵袭，并抑制肿瘤生长。此外，LINC01123靶向miR-361-3p并负向调节miR-361-3p的表达。miR-361-3p过表达可抑制HeLa和CaSki细胞的活力、迁移和侵袭。此外，miR-361-3p靶向TSPAN1并负向调节TSPAN1的表达。抑制miR-361-3p并过表达TSPAN1可逆转敲低LINC01123对HeLa细胞增殖、迁移和侵袭的影响。在CC中，敲低LINC01123通过miR-361-3p/TSPAN1调控抑制细胞增殖、迁移和侵袭，这可能为CC治疗提供一个有效的靶点。
