LAUSR

Dear Editor, Colorectal cancer (CRC) is a prevalent subtype of carcinoma which accounts for about 10% of all cancer diagnosis and is the third leading cause of cancer-related deaths globally [1].However, a great number of pathogenic factors associated with CRC development are still elusive and need further investigation. In the last several years, long non-coding RNAs (lncRNAs) were deemed to be a critical driving force for the progression of CRC [2-6], and c-Myc was discovered to be a functional partner of lncRNAs [7]. Nucleoporin 88 (NUP88) is a component of nucleoporins, which is upregulated in tumor tissues including CRC [8]. It is reported that NUP88 interacts with vimentin and protects its serine residue (Ser83) from dephosphorylation, thereby promoting cell proliferation [9]. Another form of vimentin phosphorylation, namely the phosphorylation at Ser39, results in the development of cell migration and tumor metastasis [10]. Here we report a lncRNAMILNR1, which was found to be down-regulated in CRC cells, that could regulate NUP88 in cis by interacting with c-Myc and inhibit vimentin phosphorylation and CRC growth. We first analyzed the expression levels of lncRNAs from both colon and rectum adenocarcinoma patients’ samples and their adjacent normal colorectal tissues from The Cancer Genome Atlas (TCGA) database. We found that a non-coding transcript AC087500.2 was down-regulated