Wang Wenbo, Hou Zhiliang, Wen Chengcai, Ge Liyue, Ge Lili
Department of Thoracic Surgery, Henan Provincial Chest Hospital, Zhengzhou, China.
Huai'an Second People's Hospital and The Affiliated Huai'an Hospital of Xuzhou Medical University, Huai'an, China.
Front Genet. 2020 Oct 16;11:929. doi: 10.3389/fgene.2020.00929. eCollection 2020.
Previous evidence suggests that long non-coding colon cancer-associated transcript-1(CCAT1) plays a pivotal role in the progression of a variety of tumors. However, little is known about its role in lung adenocarcinoma (LAD). In this study, we found LAD tissue samples had a higher expression of CCAT1 but a lower expression of miR-219-1 compared to their adjacent non-tumor tissues. CCAT1 negatively regulated the expression of miR-219-1. miR-219-1 suppressed the proliferation of A549 and H1299 cells. Knockdown of CCAT1 inhibited the proliferation, migration, and invasion of A549 and H1299 cells, which were reversed by the miR-219-1 inhibitor. CCAT1 knockdown increased the expression of E-cadherin but decreased the expressions of N-cadherin and vimentin, which were restored by the miR-219-1 inhibitor. , knockdown of CCAT1 suppressed the tumor growth of LAD xenografts, which were rescued by the inhibition of miR-219-1. In summary, our findings suggested that CCAT1 promotes the progression of LAD sponging miR-219-1, providing a potential therapeutic target for LAD.
先前的证据表明,长链非编码结肠癌相关转录本1(CCAT1)在多种肿瘤的进展中起关键作用。然而,其在肺腺癌(LAD)中的作用却知之甚少。在本研究中,我们发现与相邻的非肿瘤组织相比,LAD组织样本中CCAT1表达较高,但miR-219-1表达较低。CCAT1负向调节miR-219-1的表达。miR-219-1抑制A549和H1299细胞的增殖。敲低CCAT1可抑制A549和H1299细胞的增殖、迁移和侵袭,而miR-219-1抑制剂可逆转这些作用。敲低CCAT1可增加E-钙黏蛋白的表达,但降低N-钙黏蛋白和波形蛋白的表达,而miR-219-1抑制剂可使其恢复。敲低CCAT1可抑制LAD异种移植瘤的生长,而抑制miR-219-1可使其恢复。总之,我们的研究结果表明,CCAT1通过海绵化miR-219-1促进LAD的进展,为LAD提供了一个潜在的治疗靶点。