TRIM11, a direct target of miR-24-3p, promotes cell proliferation and inhibits apoptosis in colon cancer.
TRIM11, a direct target of miR-24-3p, promotes cell proliferation and inhibits apoptosis in colon cancer.
复制标题
TRIM11 是 miR-24-3p 的直接靶标，可促进结肠癌细胞增殖并抑制细胞凋亡
DOI：
10.18632/oncotarget.13550
复制
发表时间：
2016-12-27
期刊：
影响因子：
--
通讯作者：
Liu L
中科院分区：
文献类型：
--
作者：
Yin Y;Zhong J;Li SW;Li JZ;Zhou M;Chen Y;Sang Y;Liu L
TRIM 11（tripartite motif-containing protein 11）是一种E3泛素连接酶，最近被鉴定为恶性胶质瘤和肺癌的癌基因。在本研究中，我们报告了TRIM 11在结肠癌（CC）组织中的表达相对于配对的正常组织增加，并且较高的TRIM 11水平预测CC患者的总生存期（OS）和无病生存期（DFS）较差。从机制上讲，我们发现miR-24- 3 p下调有助于CC中TRIM 11的上调。我们还证明了TRIM 11过表达促进CC中的细胞增殖和集落形成并抑制细胞凋亡，而使用CRISPR/Cas9介导的基因组编辑敲低TRIM 11抑制细胞增殖并诱导细胞凋亡。体内沉默TRIM 11降低了肿瘤生长。这些发现表明，TRIM 11通过促进细胞增殖和抑制细胞凋亡促进CC进展，并且新的miR-24- 3 p/TRIM 11轴可能是治疗CC患者的有用的新靶点。
TRIM11 (tripartite motif-containing protein 11) is an E3 ubiquitin ligase recently identified as an oncogene in malignant glioma and lung cancer. In the present study, we report that expression of TRIM11 was increased in colon cancer (CC) tissue relative to paired normal tissues and that higher TRIM11 levels predicted poor overall survival (OS) and disease-free survival (DFS) in CC patients. Mechanistically, we showed that miR-24-3p downregulation contributes to TRIM11 upregulation in CC. We also demonstrated that TRIM11 overexpression promotes cell proliferation and colony formation and inhibits apoptosis in CC, while knocking down TRIM11 using CRISPR/Cas9-mediated genome editing inhibited cell proliferation and induced apoptosis. Silencing TRIM11 in vivo decreased tumor growth. These findings indicate that TRIM11 facilitates CC progression by promoting cell proliferation and inhibiting apoptosis and that the novel miR-24-3p/TRIM11 axis may be a useful new target for treating patients with CC.