SNHG11 promotes cell proliferation in colorectal cancer by forming a positive regulatory loop with c-Myc.
摘要:
Dysregulation of long non-coding RNAs (lncRNA) have long been linked to the onset and development of colorectal cancer (CRC), yet the underlying mechanisms remain elusive. Small nucleolar RNA host gene 11 (SNHG11) is a novel lncRNA with few information about its role in development and progression of CRC. Here, we found SNHG11, a highly conserved lncRNA, was commonly overexpressed in various cancer including CRC. High expression of SNHG11 correlated with poor prognosis in patients with CRC. Gain of function and loss-of function experiments showed that SNHG11 visibly promoted proliferation in CRC cells. Mechanistic assays revealed that SNHG11 interacted with Insulin-like growth factor 2 (IGF2) mRNA-binding protein 1 (IGF2BP1), thereby enhancing the interaction between IGF2BP1 and c-Myc mRNA, a well-known target of IGF2BP1. Consequently, c-Myc mRNA expression was stabilized and its downstream targets were significantly upregulated. Further investigation demonstrated that SNHG11 upregulated c-Myc which in turn transcriptionally upregulated SNHG11. Taken together, our findings suggested that reciprocal regulation of SNHG11 and c-Myc promotes cell proliferation in CRC.
收起
展开
DOI:
10.1016/j.bbrc.2020.05.002
被引量:
年份:
1970


通过 文献互助 平台发起求助,成功后即可免费获取论文全文。
求助方法1:
知识发现用户
每天可免费求助50篇
求助方法1:
关注微信公众号
每天可免费求助2篇
求助方法2:
完成求助需要支付5财富值
您目前有 1000 财富值
相似文献(135)
参考文献(0)
引证文献(10)
来源期刊
影响因子:暂无数据
JCR分区: 暂无
中科院分区:暂无