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首页> 外文期刊>Cancer Communications >Long non-coding RNA MILNR1 retards colorectal cancer growth by inhibiting c-Myc
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Long non-coding RNA MILNR1 retards colorectal cancer growth by inhibiting c-Myc

机译：长期非编码RNA MILNR1通过抑制c-myc阻碍结肠直肠癌生长

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摘要

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.
机译：结肠直肠癌（CRC）是癌症的普遍存在的亚型，占所有癌症诊断的10％左右，是全球癌症相关死亡的第三个主要原因[1]。然而，与CRC开发相关的大量致病因素是仍然难以捉摸，需要进一步调查。在过去的几年中，长期非编码RNA（LNCRNA）被认为是CRC [2-6]进展的关键驱动力，并且发现C-MYC是LNCRNA的官能合作伙伴[7]。核常素88（NUP88）是核锁素的组分，其在包括CRC [8]的肿瘤组织中上调。据报道，NUP88与Vimentin相互作用并保护其丝氨酸残基（Ser83）免受去磷酸化，从而促进细胞增殖[9]。另一种形式的Vimentin磷酸化，即SER39的磷酸化导致细胞迁移和肿瘤转移的发育[10]。在这里，我们报告了一种LNCRNA MILNR1，其被发现在CRC细胞中被测调节，其可以通过与C-MYC相互作用来调节CIS中的NUP88并抑制VIMENIN磷酸化和CRC生长。

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