Department of Medical Oncology, the Affiliated Yantai Yuhuangding Hospital of Qingdao University Medical College, Yantai, Shandong, China.
J Cell Mol Med. 2018 Sep;22(9):4034-4044. doi: 10.1111/jcmm.13483. Epub 2018 Jun 22.
We tried to identify the function of LINC01614 in lung adenocarcinoma (LUAD) and reveal its underlying mechanisms. qRT-PCR was applied to assess the expression of LINC016014 in LUAD tissues, noncancerous tissues and cells. Through colony formation assay, MTT assay and apoptosis analysis, we examined the variation of cell proliferation and apoptosis ability after silencing LINC01614. Moreover, the targeting interactions among LINC01614, miR-217 and FOXP1 were validated via luciferase reporter assay, and then, we regulated the expression of miR-217 and FOXP1 to ascertain their importance in cell proliferation and apoptosis. LINC01614 and FOXP1 were found to be up-regulated in LUAD tumours and cells, whereas miR-217 was down-regulated. The experiment showed that target-specific selectivity exists between LINC01614-miR-217 and miR-217-FOXP1 3'UTR. Furthermore, we disclosed that inhibition of LINC01614 could activate miR-217, which subsequently restrained FOXP1. It was proved that LINC01614 promoted FOXP1 by inhibiting miR-217, which ultimately stimulated the development of LUAD.
我们试图确定 LINC01614 在肺腺癌 (LUAD) 中的功能，并揭示其潜在的机制。qRT-PCR 用于评估 LUAD 组织、非癌组织和细胞中 LINC016014 的表达。通过集落形成实验、MTT 分析和凋亡分析，我们研究了沉默 LINC01614 后细胞增殖和凋亡能力的变化。此外，通过荧光素酶报告实验验证了 LINC01614、miR-217 和 FOXP1 之间的靶向相互作用，然后我们调节了 miR-217 和 FOXP1 的表达，以确定它们在细胞增殖和凋亡中的重要性。研究发现 LINC01614 和 FOXP1 在 LUAD 肿瘤和细胞中上调，而 miR-217 下调。实验表明，LINC01614-miR-217 和 miR-217-FOXP1 3'UTR 之间存在靶特异性选择性。此外，我们揭示了抑制 LINC01614 可以激活 miR-217，从而抑制 FOXP1。研究证实，LINC01614 通过抑制 miR-217 促进 FOXP1，从而最终刺激 LUAD 的发展。
