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 p...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 lncRNA MILNR1,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.展开更多
基金supported by grants from the National Natural Science Foundation of China(81972622)Anhui Province University excellent youth talent support program(No.gxyqZD2019016)+1 种基金Provincial Natural Science Foundation of Anhui(1808085QH232)Natural Science Research Projects for Universities of Anhui Province(KJ2019A0221).
文摘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 lncRNA MILNR1,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.
