Kong Qingling, Li Guangcai, Yin Gang, Li Kun, Zhang Dongqing, Xu Weihao
Hospital Infection Control Office, Rizhao People's Hospital, Rizhao 276800, China.
China-Canada International Health Management Center, Rizhao Hospital of TCM, Rizhao 276800, China.
J Oncol. 2021 Jun 5;2021:9951010. doi: 10.1155/2021/9951010. eCollection 2021.
Understanding the role of lncRNAs in the development of human malignancies is necessary for the targeted therapy of malignant tumors, including esophageal cancer (EC). Nevertheless, the specific role and regulatory mechanism of lncRNA WDFY3-AS2 in EC are still unclear. Here, we examined the functional role and regulatory mechanism of WDFY3-AS2 in EC.
RT-qPCR assay was applied to measure the expression of WDFY3-AS2 and miR-18a in EC samples and cells. The luciferase reporter and RIP assays were used to check the relationship between WDFY3-AS2, miR-18a, and PTEN. Counting Clock Kit-8 (CCK-8) assay was carried out to detect cell viability, and transwell assays were used for measuring cell migration and invasion.
Underexpression of WDFY3-AS2 was found in EC specimens and cells, which predicted a poor prognosis of EC patients. Reexpression of WDFY3-AS2 repressed the progression of EC via inhibiting cell proliferation, migration, and invasion. Additionally, WDFY3-AS2 was negatively correlated with miR-18a and positively with PTEN. Furthermore, we discovered that the expression of PTEN decreased by miR-18a mimic was rescued by WDFY3-AS2 overexpression.
WDFY3-AS2 modulates the expressional level of PTEN as a competitive endogenous RNA via sponging miR-18a in EC, which suggests that the WDFY3-AS2/miR-18a/PTEN pathway might be involved in the progression of EC.
了解长链非编码RNA(lncRNAs)在人类恶性肿瘤发生发展中的作用对于包括食管癌(EC)在内的恶性肿瘤的靶向治疗至关重要。然而,lncRNA WDFY3-AS2在EC中的具体作用和调控机制仍不清楚。在此,我们研究了WDFY3-AS2在EC中的功能作用和调控机制。
应用逆转录定量聚合酶链反应(RT-qPCR)检测EC样本和细胞中WDFY3-AS2和miR-18a的表达。采用荧光素酶报告基因和RNA免疫沉淀(RIP)实验检测WDFY3-AS2、miR-18a和磷酸酶及张力蛋白同源物(PTEN)之间的关系。进行细胞计数试剂盒-8(CCK-8)实验检测细胞活力,采用Transwell实验检测细胞迁移和侵袭能力。
在EC标本和细胞中发现WDFY3-AS2表达下调,这预示着EC患者预后不良。WDFY3-AS2的重新表达通过抑制细胞增殖、迁移和侵袭来抑制EC的进展。此外,WDFY3-AS2与miR-18a呈负相关,与PTEN呈正相关。此外,我们发现WDFY3-AS2过表达可挽救miR-18a模拟物导致的PTEN表达降低。
在EC中,WDFY3-AS2作为竞争性内源RNA通过结合miR-18a调节PTEN的表达水平,这表明WDFY3-AS2/miR-18a/PTEN通路可能参与EC的进展。