SNHG11 promotes cell proliferation in colorectal cancer by forming a positive regulatory loop with c-Myc.

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.