LncRNA LINC00511 Acts as an Oncogene in Colorectal Cancer via Sponging miR-29c-3p to Upregulate NFIA.

Abstract

BackgroundColorectal cancer (CRC), characterized by high mortality and incidence rate, is one of the most common types of rectum tumors in the gastrointestinal tract worldwide. An increasing number of investigations indicated that long noncoding RNAs (lncRNAs) have been implicated in the growth of a wide range of cancers. Although it has obtained general acceptance that lncRNA LINC00511 plays a significant role in numerous cancers, the regulatory mechanism of LINC00511 in CRC still needs to be explored.Materials and MethodsBioinformatics analysis and a wide range of experiments of sphere formation assay, cell proliferation assay, RT-qPCR, colony formation assay, Transwell assay and Western blot assays investigated the function and mechanism of LINC00511 in CRC tissues and cells.ResultsOur results manifested that the expression level of LINC00511 was obviously upregulated in CRC tissues and cells and it accelerated CRC development through facilitating cell proliferation, metastasis and stemness. Molecular mechanism exploration uncovered that LINC00511 acted as a ceRNA competing with NFIA to bind with miR-29c-3p. Through rescue experiments, we discovered that NFIA upregulation partly counteracted the inhibitive effect induced by LINC00511 silencing on CRC progression.ConclusionThese results revealed that LINC00511 participated in the progression of CRC by targeting the LINC00511/miR-29c-3p/NFIA axis, indicating that LINC00511 may be a potential therapeutic target for CRC treatment.